The Most Attractive Hyderabad Call Girls Kothapet 𖠋 9332606886 𖠋 Will You Mis...
2014 Via Christi Cardiac Symposium Presentations
1. 10/30/14
1
The Burden of
Mitral Regurgitation
Agenda
Classification & Etiology
Prevalence
Clinical Outcomes
Therapy Considerations
Key Points
§ Prevalence is age-dependent, affecting
9.3% of those aged >75 years
§ Etiology is primary (i.e., valvular) or
secondary (i.e., ventricular)
§ Excess mortality occurs from medical
management and delays in intervention
§ Surgical risk and etiology determine
intervention and its timing
Nkomo et al. Burden of Valvular Heart Diseases: A Population-based Study,
Lancet, 2006; 368: 1005-11.
Suri R et al., JAMA 2013;310:609-16
Nishimura R, et al., J Am Coll Cardiol 2014;63:2438-88
Structural Heart Disease
Increases with Age
14
12
10
8
6
4
2
0
Prevalence (%) of moderate
to severe valve disease
All valve disease
Mitral valve disease
Aortic valve disease
<45 45-54 55-64 65-74 >75
> 9.3% for ≥75 year olds (p<.0001)
Nkomo et al. Burden of Valvular Heart Diseases: A Population-based Study,
Lancet, 2006; 368: 1005-11.
Age (years)
Classification of MR – 2 Types
Incompetent mitral
valve closure
Systolic retrograde blood flow
from the LV into the LA
Mayo Clinic (www.mayoclinic.com)
Primary:
Anatomic abnormality
the mitral valve
• Leaflets
• Subvalvular
apparatus
• Chordae and
papillary muscles
Secondary :
LV dilation; often
secondary to ischemic
heart disease
• Leads to mitral
annular dilation
• Incomplete
coaptation of the
mitral valve
Classification of MR
Primary
“The Valve”
Sorajja, Paul, MD; Abbott Northwestern Hospital
Secondary
“The Ventricle”
Usually myxomatous Ischemic or not
2. 10/30/14
2
Posterior Anterior
Flai l Bi-Leaflet
Sorajja, Paul, MD; Abbott Northwestern Hospital
Prognostic Determinants
Severity
Left Ventricular Function
Symptoms
Asymptomatic DMR
Natural History
100
90
80
70
60
50
Survival %
≤1 RF
0 2 4 6 8
10
Avierinos JF, et al. Circulation 2002;106:1355
≥2 RF
95 ±2
70 ±5
55 ±9
MR ≥3
or
EF <50%
Risk Factors
Age ≥50 yrs
Atrial fibrillation
LA enlargement
Flail
Years after diagnosis
Asymptomatic Primary MR
Severity and Survival
Worse Survival
100
90
80
70
60
50
0
Survival (%)
P<0.01
ERO <20mm2 (91 ±3%)
ERO ≥40mm2 (58 ±9%)
0 1 2 3 4
Years
5
Enriquez-Sarano M et al. NEJM 2005;352:875-83
ERO 20-39mm2
(66 ±6%)
More CV Events
70
60
50
40
30
20
10
0
Rate of Cardiac Events %
P<0.01
ERO ≥40mm2 (62 ±8%)
0 1 2 3 4
Years
5
ERO <20mm2 (15 ±4%)
ERO 20-39mm2
(40 ±7%)
EF and Surgical Outcome
100
80
60
40
20
0
Survival %
0 1 2 3 4 5 6 7 8 9
Years
10
EF ≥60%
EF 50-60%
EF <50%
P=0.0001
72 ±4%
53 ±9%
32 ±12%
EF <60% is Abnormal in MR
Enriquez-Sarano M, et al., Circulation 1994;90:830-837
Symptoms and Surgery
Outcome with Primary MR
100
80
60
40
20
0
Survival %
0 1 2 3 4 5 6 7 8 9
Years
10
NYHA I-II
NYHA III-IV
P<0.0001
90 ±2
76 ±5
73 ±3
48 ±4
Tribouilly CM et al., Circulation 1999;99:400-5
3. 10/30/14
3
Flail Mitral Leaflet
Natural History
100
80
60
40
20
0
Survival %
P<0.001
0 1 2 3 4 5 6 7 8 9
Years After Diagnosis
10
Ling L, et al. N Engl J Med 1996; 335:1417-1423
Class I or II
Class III or IV
Mortality
4% per year
34% per year
Classification of MR
Primary
“The Valve”
Sorajja, Paul, MD; Abbott Northwestern Hospital
Secondary
“The Ventricle”
Usually myxomatous Ischemic or not
Secondary Mitral Regurgitation
A Ventricular Problem
• Papillary muscle
displacement
Trichon BH, et al. Am J Cardiol 2003;91:538-43
Regional or
Global Dysfunction
• Annular flattening
• Leaflet tethering
Secondary Mitral Regurgitation
A Harbinger of Poor Outcome
Secondary Mitral Regurgitation
Increased Severity = Increased Morbidity
Post-MI SOLVD (EF >35%) Hospitalization-free survival decreased
P<0.001
0 1 2 3 4
Years
0 365 730
1095
Two-fold Increase Risk of Death
1.0
0.8
0.6
0.4
0.2
0.0
Survival (%)
5
Grigioni F, et al. Circulation 2001;103:1759-64;
Basket JF, et al. Can J Cardiol 2007;23:797-800
50
40
30
20
10
0
Death or heart failure
hospitalization %
P=0.0006
Follow-up time (days)
MI w/o MR
MI with MR
61 ±6
38 ±5
Mitral
Regurgitation
No Mitral
Regurgitation
with increased MR severity1
100
80
60
40
20
0
Hospitalization-free Survival (%)
0 1 2 3 4 5 6 7
Years
P<0.01
No MR(40%)
Mild/mod MR
(25%)
Severe MR
7%)
Transplant-free survival decreased
with increased MR severity2
100
90
80
70
60
50
40
Transplant-free Survival (%)
No MR & Grade I
(82.7 ±3.1%)
Grade II
(64.4 ±4.9%)
0 500 1000 1500 2000
Days
Grade IV
(46.5 ±6.7%)
Grade III
(68.5 ±4.6%)
1. Rossi A, Dini FL, Faggiano P, et al. Independent prognostic value of functional mitral regurgitation in patients with heart failure: a quantitative analysis of 1256 patients with ischemic and
non-ischaemic dilated cardiomyopathy. Heart. 2011;97(20):1675-1680.
2. Bursi F, Barbieri A, Grigioni F, et al. Prognostic implications of functional mitral regurgitation according to the severity of the underlying chronic heart failure: a long-term
outcome study. Eur J Heart Fail. 2010;12(4):382-388.
MITRAL REGURGITATION
Untreated severe MR is
associated with increased
morbidity and mortality
What about therapy?
4. 10/30/14
4
A Largely Untreated
Patient Population
Mitral Regurgitation 2009 U.S. Prevalence
Total MR Patients1,2
Eligible for Treatment3,4
(MR Grade ≥3+)
4,100,000
1,700,000
Annual Incidence3
(MR Grade ≥3+)
Annual MV Surgery5
250,000
30,000
14% Newly Diagnosed
Each Year
Only 2% Treated Surgically
1,670,000
Untreated Large
and Growing Clinical
Unmet Need
1. US Census Bureau. Statistical Abstract of the US: 2006, Table 12.
2. Nkomo et al. Burden of Valvular Heart Diseases: A Population-based Study, Lancet, 2006; 368: 1005-11.
3. Patel et al. Mitral Regurgitation in Patients with Advanced Systolic Heart Failure, J of Cardiac Failure, 2004.
4. ACC/AHA 2008 Guidelines for the Management of Patients with Valvular Heart Disease, Circulation: 2008
5. Gammie, J et al, Trends in Mitral Valve Surgery in the United States: Results from the STS Adult Cardiac Database, Annals of Thoracic Surgery 2010.
Pathophysiology of MR
Increasing Mitral
Regurgitation
Increase Load/
Stress
Muscle Damage/
Loss
Dilation of
Left Ventricle 1 year
Dysfunction
of Left Ventricle
mortality
up to
57%1
1 Cioffi G, et al. Functional mitral regurgitation predicts 1-year mortality in elderly patients with systolic chronic heart failure.
European Journal of Heart Failure 2005 Dec;7(7):1112-7
MR and Heart Failure
Prevalence in CHF
Moderate or
severe MR
present in
∼40%
70
60
50
40
30
20
10
0
%
Advanced Heart Failure
None
Moderate
Mod-Severe
Severe
∼5 million people with heart failure in U.S.
Patel JB, et al. J Card Fail 2004;10:285-291; Go AS, et al. Circulation 2013;127:e6.
Current Therapy Considerations
Medical Therapy
Less Invasive
Increased MR Reduction
MV Surgery
MitraClip®
*Reference Source: Instructions For Use
See important safety information referenced within
General Principles of Therapy
Primary
Surgery for
symptoms or LV
dysfunction
Secondary
Asymptomatic
if repairable
and low risk
Medical
therapy first
No medical
option for valve
Consider CRT
Surgery only in
highly selected
patients with HF
Timing of Surgical Intervention
ACC/AHA Guidelines – Primary MR
Consider surgery when
Symptoms
or
LV dysfunction (EF<60%, ESD≥40 mm)
Try to repair
Nishimura R, et al., J Am Coll Cardiol 2014;63:2438-88
5. 10/30/14
5
Timing of Surgical Intervention
ACC/AHA Guidelines – Primary MR
Prophylactic Repair
Can be done if
likelihood of success >95%
and
mortality rate <1%
Nishimura R, et al., J Am Coll Cardiol 2014;63:2438-88
Early Surgery Is Better
Patients without Class I Indications
100
80
60
40
20
0
Survival %
0 5 10 15 20
Follow-up, y
Suri R et al., JAMA 2013;310:609-16
Early surgery
Medical management
Log-rank P<.001
Surgical Intervention
ACC/AHA Guidelines – Secondary MR
Surgery may be considered for
severe symptoms despite
optimal GDMT for HF (IIb)
Also for other CV surgery if
severe (IIa) or moderate (IIb)
Nishimura R, et al., J Am Coll Cardiol 2014;63:2438-88
Surgery for Secondary MR
Wu AH, et al. J Am Coll Cardiol 2005;45:381-87
0 500 1000 1500 2000
No Mortality Benefit
1.0
0.8
0.6
0.4
0.2
0.0
Event-free Survival
Time (Days)
Unoperated MR in Europe
396 patients with symptomatic severe MR
No surgery in 49%
160
140
120
100
80
60
40
20
Mirabel M, et al. Eur Heart J 2007;28:1358-1365
Predictors were
age, morbidity,
non-ischemic
etiology, MR
severity
53% degenerative
0
Decision not
to operate
Decision to
operate
P<0.0001
63% 59%
67% 42%
15%
<50 50-60 60-70 70-80 >80
Medical Management
1,095 pts with severe MR and CHF
16%
5-yr mortality for medically managed = 50%
Goel SS, et al. J Am Coll Cardiol 2014;63:185-90
DMR
84%
Surgery
Medical
FMR
36%
64%
6. 10/30/14
6
30
Percutaneous
“Minimally Invasive” Options
MitraClip® System
MitraClip® Indications
The MitraClip Clip Delivery System is indicated for the
percutaneous reduction of significant symptomatic
mitral regurgitation (MR ≥ 3+) due to primary
abnormality of the mitral apparatus [degenerative
MR] in patients who have been determined to be at
prohibitive risk for mitral valve surgery by a heart
team, which includes a cardiac surgeon experienced
in mitral valve surgery and a cardiologist experienced
in mitral valve disease, and in whom existing
comorbidities would not preclude the expected
benefit from reduction of the mitral regurgitation.
Transcatheter Mitral Repair
ACC/AHA Guidelines – Primary MR
May be considered for prohibitive risk
patients with primary MR and severe
symptoms despite GDMT (class IIb)
MitraClip® System MitraClip® Experience
§ EVEREST I Feasibility (n=55)
§ EVEREST II Pivotal
§ Pre-Randomization (n=60)
§ HR Registry (n= 78)
§ Randomized (2:1 Clip to Surgery) (n= 279)
§ REALISM Registry
Continued Access (n=965)
§ Worldwide Commercial Use:
>15,000 patients
7. 10/30/14
7
Prohibitive Surgical Risk
DMR Cohort (n=127)
Age: 82 ±9 years
Prior MI: 24%
Prior stroke: 10%
Diabetes: 30%
COPD: 32%
Renal disease: 28%
Mean STS Risk
13.2%
Lim et al. Improved functional status and quality of life in prohibitive surgical risk
patients with degenerative mitral regurgitation after transcatheter mitral valve repair,
JACC 2014;64:182-192.
Prohibitive Surgical Risk
DMR Cohort (n=127)
95% implant success
No procedural deaths
LOS = 2.9 days
1.0
0.8
0.6
0.4
0.2
0.0
Event Free Survival
(N=127)
0 100 200 300 400
Days Post Index Procedure
Lim et al. Improved functional status and quality of life in
prohibitive surgical risk patients with degenerative mitral
regurgitation after transcatheter mitral valve repair, JACC 2014;64:182-192.
Prohibitive Surgical Risk
DMR Cohort (n=127)
Hospitalizations for Heart Failure
0.67
73% Reduction
1
Year
Prior… 1
Year
Post…
Left Ventricular Volumes
0.18
1.0
0.8
0.6
0.4
0.2
0.0
HF
Hospitalization
Rate
per
Patient
Year
Left Ventricular End Diastolic Volume Left Ventricular End Systolic Volume
125
-16 mL
109
140
130
120
110
100
90
80
70
60
Baseline 1 Year
Volume
mL
≈
49
60
55
50
45
40
35
Paired (N = 69)
Data (N=69)
46
30
Baseline 1 Year
≈
-3 mL
1+
2+
Clinically 3+
Important Reduction
2+ 4+
Mitral Regurgitation Grade
1+
2+
3+
4+
100%
80%
60%
40%
20%
0%
Baseline 12 Months
Patients (%)
100%
80%
Clinically 60%
Important ImprovIeII ment
40%
20%
Source: MitraClip Clip Delivery System Instructions for Use.
See important safety information referenced within.
0
1+
3+
4+
of Mitral Regurgitation
IV
IV IV
III
III III
II
II
II
I
I I
0%
Baseline 30 Days 12 Months
Patients (%)
NYHA Functional Class
I
II
IV
in NYHA Functional Class
Clinically Important Reduction
in the Rate of Hospitalization
for Heart Failure
Clinically Important Reverse
LV Remodeling
Summary
§ MitraClip® therapy safely reduces DMR in patients
at prohibitive risk for MV surgery
§ In this group of prohibitive risk DMR patients,
MitraClip therapy provides meaningful clinical
improvements
§ Reduction of LV volumes
§ Improvements in NYHA Functional Class
§ Improvements in Quality of Life
§ Reduction in Hospitalizations for Heart Failure
Source: MitraClip Clip Delivery System Instructions for Use.
See important safety information referenced within.
Key Points
§ Prevalence is age-dependent, affecting
9.3% of those aged >75 years
§ Etiology is primary (i.e., valvular) or
secondary (i.e., ventricular)
§ Excess mortality occurs from medical
management and delays in intervention
§ Surgical risk and etiology determine
intervention and its timing
CLINICAL TRIALS
8. 10/30/14
8
Purpose
§ COAPT is a landmark trial to further study the
MitraClip device in symptomatic FMR patients
with heart failure
§ The study will generate important clinical and
economic data to support reimbursement and
evidence to support the development of
treatment guidelines
§ COAPT is the first randomized controlled clinical
trial to compare non-surgical (medical) standard
of care treatment to a percutaneous intervention
to reduce MR
Clinical Investigational Plan 11-512:
Version 5.1, November 11, 2013. COAPT
protocol approved by FDA July 27, 2012
Objective
To evaluate the safety and effectiveness
of the MitraClip System for treatment of
functional mitral regurgitation (FMR ≥3+)
in symptomatic heart failure subjects
who are treated per standard of care
and who have been determined by the
site’s local heart team as not
appropriate for mitral valve surgery
Clinical Investigational Plan 11-512:
Version 5.1, November 11, 2013. COAPT
protocol approved by FDA July 27, 2012
Trial Design
Goals: 430 patients at up to 75 US sites
Significant FMR (≥3+ by core lab)
Symptomatic heart failure subjects who are treated per standard of care
Determined by the site’s local heart team as not appropriate for mitral valve surgery
Specific valve anatomic criteria
Randomize 1:1
Control group
Standard of care
Clinical and TTE follow-up:
N=215
MitraClip
N=215
Baseline, Treatment, 1-week (phone)
1, 6, 12, 18, 24, 36, 48, 60 months
Clinical Investigational Plan 11-512:
Version 5.1, November 11, 2013. COAPT
protocol approved by FDA July 27, 2012
THANK YOU
9. Procedures to reduce
strokes
“LAA Occluders”
10/24/14
Dhaval Parikh MD, B.Tech, FACC
Cardiovascular Consultants of
Kansas, Wichita
10. Source of clot
and Thrombo
embolism
Neuro
hormonal
regulator
Source of
cardiac
arrhythmias
Cardiac
Reservoir
Electrical
Exclusion
Mechanical
Exclusion
11. Source of clot
and Thrombo
embolism
Source of
cardiac
arrhythmias
Neuro
hormonal
regulator
Cardiac
Reservoir
The Good
The Bad
12. LAA obliteration systems in discussion
Features Atriclip Watchman Lariat SJM Plug
Maker Atricure Atritech (Boston
scientific)
Senterheart St. Jude Medical
Approval CE and FDA CE and FDA CE and FDA CE
Approach Epicardial Endocardial Endo+Epicardial Endocardial
Type Deployable Deployable Suture ligature Deployable
Structure
Hardware left in
the heart
Yes Yes No Yes
If used in prior
open heart Sx
Yes (Possible) Yes No Yes
If retrievable
once deployed
No Yes No Yes
13. Benefit of LAA Closure
AF, Hx TE, No OAC
AF, No TE, No OAC
AF, Hx TE, OAC
AF, No TE, OAC
AF, No Risk, No TE, No OAC
Post maze, No OAC, No LAA
Cox J., et al. J Thorac Cardiovasc Surg
1999;118:833-840
14. LAA is an
important
reservoir for
thrombus
formation in
patients with AF
18. AF+LAA = Thromboembolization??
• More than 15% of
cerebral ischemia
is due to AF
• In pts with AF
and left atrial
clots more than
90 -99% are in
the LAA
• 57% of thrombi in
valvular AF
occurred in LAA
20. Silent cerebral ischemia burden was related to LAA complexity 30.8% and
17.3% patients with cactus,30.5% and 22.0% with chickenwing,13.9%
and 27.7% with windsock,and 16.7% and 38.9% with cauliflower LAA
morphologies were in the first and fourth quartiles of number of SCI per
patient, respectively (P=0.035). After adjustment for potential
confounders, only age (β 0.12; 95% CI 0.08–0.16; P<0.001),
chickenwing (β =0.28; 95% CI =0.51 to 0.04; P =0.021), windsock (β
0.38; 95%CI 0.12– 0.65; P=0.005), and cauliflower (β 0.61; 95% CI
0.07–1.14; P =0.026) LAA morphologies were significantly related to
Silent cerebral ischemia burden.
Heart Rhythm2014;11:2–7
22. Mechanisms of
thrombogenesis in
AF and LAA -
Virchow’s Triad
Revisited
1. Endothelial
changes
2. LAA dysfunction
– fibroelastic
changes
3. Local and
Lancet, 373(9658), Watson et al.,
systemic factors
23. Thrombogenic
Mechanical
Factors
• LAA volume >34
cm3
• LAA EF of < 21
• LAA anterograde
flow velocity of <20
cm/sec
• Wider LAA
neck/ostium
• Higher level of
trabeculation
24. Does Left Atrial Appendage Exclusion
Decrease the Risk of Stroke?
25. Amplatzer Cardiac Plug
Post-Market EU Observational
Study
• Sample size:
• 204 pts with non-valvular AF
• Objectives:
• Evaluate device performance and
assess AEs
• Follow up visits:
• Baseline, Procedure, Discharge, 1 & 6
months post procedure
• Rigorously executed with high level of data
quality and integrity:
• 100% of reported data has been
monitored
• Independent committee adjudicates all
AEs
• Status:
• Enrollment completed September 2011
• 15 participating centers from Germany,
Spain, UK, Ireland and Czech Republic
• Final report on 204 pts, 1214 patient
follow-up months
26. Results
Success Rates
• 96.6% (197/204) of patients
attempted were successfully
implanted
• In 89.2% of subjects, first device
selected was implanted
• Closure rate*
• At implant: 99.5%
• At 6 months: 98.9%
• No leaks were > 5 mm
• Closure rates remain consistent at
TEE evaluation from implant
through 6M follow up
* Closure Rate defined as absence of flow or flow < 3 mm jet into the LAA
27. ACP Safety data
* Closure Rate defined as absence of flow or flow < 3 mm jet into
the LAA
Event
≤7 Days
Post
Procedure
>7 days
Post
Procedur
e
Total
Peri-procedural
Stroke / TIA*
0 (0.0%) 0 (0.0%) 0 (0.0%)
Serious
Pericardial
Effusion
3 (1.5%) 0 (0.0%) 3 (1.5%)
Device
Embolization
3 (1.5%) 0 (0.0%) 3 (1.5%)
Device Related
Thrombus
0 (0.0%) 5 (2.4%) 5 (2.4%)
Total Safety
Events
6 (2.9%) 5 (2.4%)
11
(5.4%)
28.
29.
30. Summary of WATCHMAN® efficacy, safety and closure
end points
PROTECT AF1,2 CAP2 ASAP3,4 PREVAIL
Control Patients able to take warfarin
Warfarin
contraindicated
patients
1. Holmes DR et al. Lancet 2009;374:534–42 2. Reddy VY et al. Circulation. 2011;123:417-424
3. Sievert H. TCT 2011 4. Reddy, ASAP WATCHMAN, HRS 2012
Patients able to
take warfarin
Primary Endpoint
All stroke, systemic
embolism and
cardiovascular death
All stroke,
systemic
embolism and
cardiovascular
death
All stroke, systemic
embolism, and
cardiovascular
death
All stroke,
systemic
embolism and
cardiovascular
death
Mean age /CHADS 72/2.2 74/2.4 72.4/2.8 74/2.6
Total Enrolled
707 randomized1,
460 150 461
Subjects
93 pts rolled in2 Total Patients
Implanted
5422 437 142
Implantation Success 89.5%2 95.0% 94.7% 96%
Warfarin
discontinuation at 45
days
86.6% 94.9% No warfarin used >90%
Stroke
Rate ratio 0.71 (0.35–
1.64)
[Hemorrhagic Stroke:
0.09 (0.00–0.45)]
Reduction in
procedure related
stroke vs
PROTECT AF
Decreased rate of
stroke by 77% vs.
expected rate per
CHADS₂ Score
0.061% with risk
ratio of 1.07. Non
inferior to warfrain
32. Clinical Results – PLACE I
Total
Patients
N=13
AF History Persistent 12 (92%)
Flutter 1 ( 8%)
Age Avg: 57.3; Hi 64, Low
43
Sex M = 8 (62%)
Type
Procedure
LAA w/ MVR 2
(15%)
LAA w/ ablation 10
(77%)
Ablation w/ LAA 1 (
8%)
Type
Access
Median Sternotomy 2
(15%)
Minimally Invasive 2
(15%)
Percutaneous 9
(70%)
Intent to
Treat
12/13 (92%)
Acute
Closure
12/12 (100%)
Pre-LARIAT EndoCATH in LAA Post LARIAT
Heart Rhythm: 2011:8:188 - 193
No LAA
33. PLACE II
Variables N=89 N (%)
Intent-to-Treat 85 (96%)
Procedural
Closure
82 (95%)
>60day Closure w
TEE
81 (95%)
Mean CHADS2
Score
1.9+0.95
Complications
Device Related
Procedure
0
Access Related
Procedure
3 (3%)
All Death 2 (2%)
All Stroke 2 (2%)
Major Bleeding 0
Pericardial/Pleura
l Effusion
1 (1%)
J Am Coll Cardiol. 2013 Jul 9;62(2):108-18. doi: 10.1016/j.jacc.2012.06.046. Epub
2012 Oct 10
34. Clinical Variables
N=21
N(%)
Intent-to-Treat 20 (95%)
Procedural Closure 19* (95%)
>60day Closure w
TEE
16** (94%)
Mean CHADS2 Score 3.2+1.2
Complications
Device Related
Procedure
0
Access Related
Procedure
1 (5%)
All Death 1 (5%)
All Stroke 2 (10%)
Major Bleeding 0
Pericardial/Pleural
Effusion
3 (15%)
LAA
No LAA
Pre-LARIAT CT 2.5 mo. Post-LARIAT CT
** Two patients refused f/u TEE. One pt died >50d post procedure due to unrelated * <1mm leak. multiple organ failure. Am J Card, 2013
35. What is the evidence behind effective
closure?
• Multicenter
observational
study
• Leaks are always
concentric in Lariat
(Gunny Sack
Effect) and
eccentric with
Watchman (Edge
Effect)
• There was no
correlation
between the
presence of a leak
and thrombus at
the site and it
seems to be
coincidental
• Big leaks are rare
with both devices
Mean f/u 9
months
Mean f/u 12
months
36. Current evidence
• Watchman most studied and the other two need
more vetted with more data
• One third Watchman pts have some peri device
leak
• Leak rates and severity seem to be lower with
ACP and Lariat
• All three devices seem to have a good safety
profile
• The primary efficacy of watchman is comparable
to warfarin
• Long term data for all devices is yet to be
generated
37. LAA is an
important source
of arrhythmia
initiation and
maintenance
42. What does LAA electrical exclusion do
to atrial arrhythmias?
• Elimination of
triggers
• Elimination of
reentry
Triggers
• Reduction in
atrial volume
• Substrate
reduction for AF
perpetuation
Substrate
• Alteration of
RAAS
• Effect of
cardiac GP??
Autonomics
43. What can LAA
exclusion do?
Reduce
Arrhythmia
burden
Improve risk
of stroke
LAA
Exclusion
Positively
alter the
RAAS, lipid
and
glucose
metabolism
Improve LA
reservoir/
conduit function
55. MI Patient Knowledge – Greater Knowledge
Sample Items Correct
Answer
Study 1
% Patients
Study 2
% Patients
1 mo/1 yr
Study 2
% Partners
1 mo/1 yr
A normal response during sex is an increased HR, BP, and rate
of breathing
True 81% 90/89% 88/91%
If you have chest pain during sex, you should stop and rest True 80% 86/87% 89/85%
Not being able to sleep after intercourse or extreme fatigue the
False 73% 72/65% 70/74%
day after is normal
A good way to ease back into sex is to talk with your partner
about your feelings about the heart attack while taking a daily
walk
True 48% 75/66% 70/72%
Nilsson et al. Clin Nurs Res. 2012; 21:486-494; Brännstrӧm et al. J Cardiovasc Nurs 2014; 29:332-339
(references also for next slide)
56. MI Patient Knowledge – Less Knowledge
Sample Items Correct
Answer
Study 1
% Patients
Study 2
% Patients
1 mo/1 yr
Study 2
% Partners
1 mo/1 yr
WHEN TO RESUME SEX
Sex can generally be safely resumed within a few weeks
after the heart attack
True 32%
57/58% 50/45%
WARNING SIGNS
A danger sign to report to the physician is shortness of
breath or increased heart rate (pulse) for more than 15
min after intercourse
True 25% 32/36% 39/47%
Palpitations (rapid heart beating) lasting more than 15
min after intercourse are normal
False 42% 57/63% 53/55%
SAFETY CONCERNS
Wait 2 to 3 hours after a heavy meal before having sex True 36% 25/23% 26/34%
If you think a medicine is causing a problem with sex, you
False 32% 50/54% 41/40%
should stop it immediately
59. Role of Comorbidities & Sexual Concerns
Steinke et al. Europ J Cariovasc Nurs Online before print, Dec. 23, 2013
60. Overview of sexual effects of common
cardiac drugs
Drug Class Effect Notes
β – blockers Negative Exception: nebivolol
Cardiac glycosides Negative
Diuretics Negative Exception: potassium sparing
diuretics
α – blockers No effect
ACE inhibitors No effect
Calcium channel blockers No effect
Angiotensin receptor blockers Positive effect
Statins Positive effect
Nicolai et al. Neth H J 2014; 22:11-19; systematic review
61. ED, loss of sexual desire
Beta
Blockers
More SD w/ nonselective β 1 & 2
Nebivolol + effects
NS effects – metoprolol, propanolol,
acebutolol, atenolol (Nicolai et al. , 2014)
SD – BB 22% vs. 17% placebo
Impotence in men – RR 1.22
W/D BB – SD – 1.3% vs. o.3%
NS by generation of BB
(Ko et al. 2002)
Women – metoprolol neg.
affected FSFI scores
Systematic Reviews: Clayton & Ramamurthy. Adv Psychosom Med 2008; 29:70-88; Ko et al. JAMA 2002; 288:351-357; Nicolai et al. Neth H
J 2014; 22:11-19
62. Diuretics
Thiazides
• Loss of libido, ED; decreased
vaginal lubrication
• Dose related?
• bendroflumethiazide SD=22.6%
• chlorthalidone - 28% worsened ED
• ED?
• Dialysis patients – greater odds of SD
with loop diuretics (OR 1.24) (Bailie et al)
• Loop diuretics (p=0.004) and diuretics
in general (p0.003) less sexually active
(Steinke et al. 2014, Unpub.)
Aldosterone Antagonists
Spironolactone
Breast tenderness, gynecomastia,
ED; menstrual abnormalities
Higher doses = more side effects
Eplerenone
Loop Diuretics
• Nicolai et al. review –
diuretics in general
• 3 studies - neutral
effects (1998, 1999, 2006)
Less sexual side effects
• 11 studies - negative
Impotence and gynecomastia
Less menstrual problems, breast
tenderness
effects (1973-2000, 2011)
Abuannadi, O’Keefe. J Cardiovasc Pharm Therapuetics 2010; 15: 318-325; Baumhakel et al. Int J Clin Pract 2011; 65:289-298; Nicolai et al.
Neth H J 2014; 22:11-19
63. Ace inhibitors
19%
% Sexual Dysfunction
43% 42%
50%
60%
50%
40%
30%
20%
10%
0%
None BB & BB+ACEI ACEI Unknown
% Sexual Dysfunction
Those with BB and BB with ACEI – OR 3.13 for
sexual dysfunction (p=0.045) (Cook et al.)
Doumas et al. J Hypertens 2006; 24: 2387-2392; Nicolai et al. Neth H J 2014; 22:11-19; Cook et al. Am J Cardiol 2008; 102:1728-1730;
64. Angiotensin II receptors antagonists
Baumhakel et al. Int J Clin Pract 2011; 65:289-298; Nicolai et al. Neth H J 2014; 22:11-19
65. Calcium channel blockers
CARDIAC GLYCOSIDES
Baumhakel et al. Int J Clin Pract 2011; 65:289-298; Nicolai et al. Neth H J 2014; 22:11-19; Mohammadi et al. ARYA Atheroscl J 2012;
8:63-69.
66. Statins
Greater effect than
lifestyle modification!!
Kostis JB, Dobrzynski JM. ACC Annual Scientific Session, Mar 29, 2014; Nicolai et al. Neth H J 2014; 22:11-19
74. Sexual Problems in CVD by Age & Gender
Problem Age <40 yrs
(Men n=3, Women
n=10)
Ages 40-49 yrs
(Men n=33,
Women=15)
50+ yrs
(Men n=75, Women
n=17)
Reduced sexual desire Women – 50%
Men – 0%
Women – 53%
Men – 21%
Women – 65%
Men – 28%
Problems w/ orgasm Women – 10%
Men – 33%
Women – 20%
Men – 6%
Women – 12%
Men – 7%
Pain during
intercourse
Women – 10%
Men – 33%
Women – 13%
Men – 3%
Women – 12%
Men – 1%
Premature ejaculation Men – 10% Men – 25% Men – 12%
Late ejaculation Men – 0% Men – 0% Men – 1%
Erectile dysfunction Men – 33% Men - 64% Men – 63%
Vaginal dryness Women – 30% Women – 20% Women – 29%
Traeen & Olsen. Sex Relation Therapy, 2007; 22:193-208
75. Sexual Dysfunction in Heart Failure
Women Men
FSD or ED 87% 84%
Reduced desire 87% 76%
Orgasmic Problems 62% 73%
Dissatisfaction 83% 80%
Decreased vaginal lubrication 80%
Decreased lubrication + pain 50%
Unsuccessful or interrupted
76%
intercourse
Schwarz et al. Internat J Impot Res, 2008; 20,85-91
76. Prevalence of Erectile Dysfunction - HF
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
Hoekstra et al.
2012
Mohammadi et
al. 2012
Hebert et al.
2010
ED or Sexual Dysfunction
Apostolo et al.
2009
Medina 2009 Schwaarz 2008 Bohm et al. 2007 Jaarsma 2002
77. Sexual Function – Women with Congenital Heart
Disease (n=254)
Opić et al. Internat J Cardiol 2013; 168, 3872-3877
78. Sexual Function – Men with Congenital Heart
Disease
Opić et al. Internat J Cardiol
2013; 168, 3872-3877
79. The Other ED – Endothelial Dysfunction
• Which comes first?
Nehra et al. Mayo Clin Proc. 2012; 87:766-778; Montorsi et al. Eur Urol. 2003; 44:360-365; Araujo et al. J Sex Med. 2009; 6:2445-54
81. E.D.
Erectile
Dysfunction
EDucation
Early
Detection
Endothelial
Dysfunction
Early Death
Used with permission: Dr. Graham Jackson, Consulting Cardiologist, London Bridge Hospital.
85. What are the risks with sex? Low Risk
• Fewer than 3 CV risk factors, asymptomatic (AHA Class IIa, LOE C)
Levine et al. Circulation 2012; 125: 1058-72; Kostis et al. Am J Cardiol 2005; 96:313-321; Nehra et al.
Mayo Clin Proceed 2012; 87:766-778
86. What are the risks with sex? High Risk
• Thorough evaluation and stabilization before sexual activity can be
recommended (AHA Class III, LOE C)
87. What are the risks?
Indeterminate/Intermediate
• Cardiac evaluation; exercise stress testing may be useful or
required (AHA Class III, LOE C)
88. Sexual Activity Post-Cardiac Event
• Recommendations vary by:
• Sexual assessment important
• Defining sexual activity and CVD
89. Sexual Activity Recommendations
Diagnosis/Condition Recommendation
Angina Depends on stability
• Mild, stable – low risk for CV events (Class IIa, LOE B)
• Unstable, refractory – high risk, exercise testing (Class III, LOE C)
MI Prior MI (Class IIa, LOE B-C)
• Asymptomatic with mild to moderate physical activity (3-5 METs)
• No ischemia with exercise testing
• Successful coronary revascularization
Complicated MI – further evaluation
Sexual activity recommendation
• 1 – 4 weeks post-MI
Post-PCI Sexual activity recommendation
• Complete revascularization, “within days of PCI”
• Vascular complication or incomplete revascularization – further evaluation
(Class IIb, LOE C)
Levine et al. Circulation, 2012; 125:1058-1072
90. Sexual Activity Recommendations
Diagnosis/Condition Recommendation
Post-Surgical
revascularization
CABG with median sternotomy
• Sexual activity recommendation – 6-8 weeks (Class IIa, LOE B)
• Avoid positions that add strain
Minimal access cardiac surgery or robotic assisted surgery
• May return to sexual activity sooner
Heart Failure Needs to be stabilized and optimally managed
Sexual activity recommendation (Class IIa/III, LOE B-C)
• Reasonable if compensated and/or mild HF, NYHA Class I or II
• Not advised for decompensated or advanced HF, NYHA Class III or IV
Valvular Heart Disease Depends on condition
• Mild to moderate/no or mild symptoms/valvular repair or replacement –
may resume (Class IIa, LOE C)
• Severe disease or significant symptoms – optimal management, exercise
testing (Class III, LOE C)
Levine et al. Circulation, 2012; 125:1058-1072
91. Sexual Activity Recommendations
Diagnosis/Condition Recommendation
Pacemakers
ICD
Arrhythmias
Those with arrhythmias and safe for leisure or moderate (3-5 METs) sporting
activities – safe for sexual activity (Class IIa, LOE C)
• Atrial fibrillation or flutter, well controlled ventricular response
• HX of AV nodal reentrant tachycardia, AV reentry tachycardia, or atrial
tachycardia w/ controlled arrhythmias
• A pacemaker
• ICD implanted for primary prevention without multiple shocks appropriate to
the particular arrhythmia
• ICD for secondary prevention, physical activity does not precipitate ventricular
tachycardia or ventricular fibrillation and has not received frequent appropriate
shocks
Congenital Heart Disease
Sexual activity reasonable if the following is not present:
• Decompensated or advanced HF
• Severe or significant valvular disease with symptoms
• Uncontrolled arrhythmias (Class IIa, LOE C)
Hypertrophic
Cardiomopathy
Sexual activity reasonable for most patients (Class IIa, LOE C)
• Deferred with severe symptoms until stabilized
Levine et al. Circulation, 2012; 125:1058-1072
98. Sexual Quality of Life - CABG
(Lai et al. J Cardiovasc Nurs 2011; 26:487-496)
99. Path Model – Information, Fear, Sexual
Interest
Patient Fear of
Sexual Activity
-0.33* -0.40*
Model – 37% variance sexual
interest
Indirect effect – 42% of
total effect of info by
providers on sexual interest
Sexual Interest
Information by
Provider
0.18
β=0.13, Sobel Z=1.96,
p=0.05; 95% CI=0.01-0.26
100. Sexual Counseling – Transplantation, LVAD
Steinke et al. Circulation. 2013;128:10.1016/CIR.0b013e31829c2e53; Phan et al. J Sex Med. 2010; 7:2765-2773; Marcuccilli et al. J Cardiovasc Nurs. 2011;
26:504-511; Samuels et al. J Thoracic Cardiovasc Surg. 2004; 127:1432-1435.
109. Interventional Approaches
Verbal Information
• Lecture/dialogue
Written Information
• Brochure
• Booklet
Visual Information
• Video
• Other Media
Seminar discussion
• Lifestyle
• Risks
Practical Training
• Physical
• Stress Mgmt
114. Imperatives In Stroke:
Ischemic and Hemorrhagic
Stroke Guidelines Update
James Walker, MD
Medical Director Neurocritical Care and Stroke
Via Christi Hospitals, Wichita, KS
115. Goals and Objectives
Introduce Emergency Neurologic Life Support (ENLS) course
offered by Neurocritical Care Society
Review initial management of acute ischemic stroke (AIS)
based on 2013 AHA/ASA Guidelines
Review initial management extracranial carotid and vertebral
artery disease based on 2011 AHA/ASA Guidelines
Review initial management of spontaneous intracerebral
hemorrhage (ICH) based on 2010 AHA/ASA Guidelines (update
due)
Review initial management of aneurysmal subarachnoid
hemorrhage (SAH) based on 2012 AHA/ASA Guidelines and 2011
NCS Consensus Conference Recommendations
116.
117. Emergency Neurologic Life
Support (ENLS)
Protocols for 13 neurologic emergencies (AIS, ICH, SAH,
SE, TBI, SCI, Meningitis/Encephalitis, etc)
Initial stabilization, management, and communication
algorithms
Created by Neurocritical Care and Emergency physicians
Designed for physicians, critical care nurses, or other
professionals that treat neurologic emergencies
CME available: http://enls.neurocriticalcare.org
118. Overview of Guideline
Sources
AHA/ASA- American Heart Association/American Stroke
Association
13-15 Experts on each topic (AIS/SAH/ICH)
Cardiology, Emergency Medicine, Interventional
Neuroradiology, Vascular Neurology, Neurosurgery,
Neurocritical care, Rehabilitation, Nursing
Utilize the “Level of Evidence”(LOE) grading algorithm
NCS- Neurocritical Care Society
20-25 Experts (SAH only)
Neurosurgery, Neurocritical care, Neurology, Interventional
Neuroradiology, Neuroanesthesia
Utilize the “GRADE” system
121. The GRADE System
Grades of Recommendation Assessment,
Development and Evaluation
Distinguishes “strength” of guideline versus
“quality” of evidence
Adopted by many national and international
professional medical societies, health-related
branches of government, health care regulatory
bodies, and UpToDate
Kavanagh BP (Sept 2009) The GRADE System for Rating Clinical Guidelines. PLoS Med 6(9): e1000094.
doi:10.1371/journal.pmed.1000094
Atkins D, Best D, Briss PA, Eccles M, Falck- Ytter Y, et al. (2004) Grading quality of evidence and strength of recommendations. BMJ
328: 1490.
122. Stroke Facts and Stats
4th leading cause of death in US since 2008
80-85% AIS / 15-20% ICH or SAH
PUBLIC EDUCATION ESSENTIAL/INADEQUATE
<50% of 911 calls occur within 1 hr of symptom onset- less
than half attribute symptoms to stroke (Stroke.
2007;38:361–366)
Fibrinolytic use could increase from <5% to nearly 30% if
pts arrived early enough (Neurology. 2005;64:654–659)
Only 53% use EMS (J Vasc Interv Neurol. 2008;1: 83–86)
124. Ischemic Stroke
Embolic
Blood clot or plaque forms
in the body and travels
through the blood stream
to the brain
Thrombotic
Fatty deposits develop in
the lining of the blood
vessel wall which narrows
the blood vessel
125. Acute Ischemic Stroke
Penumbra
Salvageable
ischemic brain
Time is critical
“Golden Hour of
Stroke”
128. EMS Goals and Prehospital
Management (general)
Rapid evaluation of ABCs
Early stabilization
Neurological evaluation (Class I; LOE: B)
Cincinnati Prehospital Stroke Scale
Rapid transport and triage to stroke-ready
hospital- Prehospital notification (Class I; LOE: A)
DETERMINE “LAST KNOWN WELL” (LKW)
Circulation. 2011;124:e404]. Circulation. 2010;122(suppl 3):S818–S828.
129. EMS Goals and Prehospital
Management (specific)
Supplemental oxygen TKS > 94%
Establish IV access
Blood pressure management
Fluid administration (not excessive) +/- head of
stretcher flat for SPB<120
Antihypertensive meds for SBP>220 (if directed)
Glucose testing!!!
IV glucose if <60 mg/dL
ESTABLISH TIME LKW and family contact
Stroke. 2013;44:XXX-XXX
130. ED Management of AIS
Rapid identification
Neurologic assessment (NIH Stroke Scale)
Labs
ALL- glucose, electrolytes/Cr, PTT/INR, CBC/plts,
troponin
SELECT- Tox/ETOH, HCG, ABG,LFTs
Imaging (noncontrast head CT)
135. TPA Eligibility Checklist
Patient Selection Criteria:
Age > 18
Ischemic stroke with a measureable
neurological deficit
Time “Last Known Well” (LKW) < 4.5 hours
Contraindications for extending to 3 – 4.5 hours
History of stroke AND diabetes
History of OAC use (regardless of INR)
Age > 80
NIHSS > 25
136. TPA-Absolute Contraindications
ICH/SAH (currently or any history)
Major early infarct signs (hypodensity) on CT
Internal bleeding within last 3 weeks
Known bleeding diathesis:
Platelet < 100,000
Heparin within 48 hours and elevated PTT
PT > 15 sec or INR > 1.7
Currently taking Dabigatran
Stroke, serious head trauma, intracranial/intraspinal
surgery within 3 months
Unable to obtain BP < 185/110, despite treatment
Known intracranial neoplasm, AVM, or aneurysm
137. TPA-Warnings
Acute pericarditis
Known subacute
bacterial endocarditis
Significant hepatic or
renal dysfunction
Pregnant
Childbirth within 30 days
Hemorrhagic ophthalmic
conditions
AMI within last 3 months
Seizure at onset
Minor or rapidly improving
symptoms
Severe neurological deficits
(e.g., NIHSS > 22)
Currently on OACs
Major surgery within 2 wks
Arterial puncture at non-compressible
site
Lumbar puncture in last
week
Abnormal blood glucose (<
50 or > 400)
138. Fibrinolytics
Intravenous rtPA is THE ONLY FDA APPROVED
fibrinolytic for AIS within 3 hrs (Class I; LOE: A) to 4.5
hrs (Class I; LOE: B) of symptom onset
The usefulness of intravenous administration of
other fibrinolytic or defibrinogenating agents is not
well established, and they should only be used in the
setting of a clinical trial (Class IIb; LOE: B)
Intravenous streptokinase for AIS is not
recommended (Class III; LOE: A)
Stroke. 2013;44:XXX-XXX
140. Safety of TPA in Stroke Mimics
Mimics identified in 3-21% of rtPA treated patients
Seizures
Conversion disorder
Complicated migraine
No evidence of increased risk or symptomatic
hemorrhage
Stroke. 2009;40:1522–1525
Ann Emerg Med. 2003;42:611–618
Neurology. 2010;74:1340–1345
141. Safety of “Community
Models” of Stroke Care
risk
sICH, in-hospital mortality (JAMA 2000;283:1151–1158)
in-hospital mortality(Arch Intern Med.
2002;162:1994–2001)
No increased risk (Stroke. 2010;41:2098–2101)
No increased risk (Acad Emerg Med. 2010;17:1062–
1071)
BOTTOM LINE- CONTINUING TO BECOME SAFER
142. Treatment of Hypertension in AIS Thrombolytic
Candidates
Management of BP prior to rtPA (goal >185/110 mm Hg)
Labetalol 10–20 mg IV
Nicardipine 5 mg/h IV, titrate to max 15 mg/h
Consider hydralazine, esmolol, enalaprilat, etc
If BP is not maintained at or below 185/110 mm Hg, DO NOT
administer rtPA
Management of BP during and after rtPA (goal < 180/105 mm Hg)
Labetalol 10 mg IV followed by continuous infusion 2–8 mg/min
Nicardipine 5 mg/h IV, titrate to max 15 mg/h
Esmolol 50-300 mcg/kg/min
If BP not controlled or diastolic BP >140 mm Hg, consider IV sodium
nitroprusside (Class I; LOE: B)
Stroke. 2013;44:XXX-XXX
143. Summary of ED Management
for AIS
Rapid assessment and history- Determine “LKW”
Labs- glucose*, plt, INR, troponin, Cr (Class I; LOE: B)
Neuro exam using NIHSS (Class I; LOE: B)
Non-contrast head CT
TPA checklist (if no hemorrhage on CT)
BP must be <185/110 to receive rtPA (Class I; LOE: B)
Phone consultation w PSC/CSC stroke physician
144. Summary of ED
Management for AIS (cont)
Fibrinolytic given
Consider fluid bolus
Maintain strict BP control
<180/105
Class I; LOE: B
rtPA Complications
Bleeding
Angioedema (1-5%)
No fibrinolytic given
Consider ASA 325mg
Consider fluid bolus
BP management first 24 hrs
Lower by 15% only if
>220/120
Withhold treatment if
<220/120
Class 1; LOE: C
Stroke. 2013;44:XXX-XXX
145. Interhospital Transport
“Drip (tPA) and Ship” ischemic stroke patients
“Ship” ischemic stroke patients with LKW >4.5 and <8 hrs
(potential intraarterial therapy)
Maintain contact with medical command/receiving hospital
Adhere strictly to blood pressure guidelines
Assess constantly for clinical deterioration
Maintain aspiration precautions
Supplemental oxygen TKS>94% (Class 1; LOE: C)
Stroke. 2013;44:XXX-XXX
146. IA Stroke Therapy
Pharmacotherapy
rtPA
Urokinase
Tenecteplase
Retivase
ReoPro
Mechanical Clot Retrieval (with / without pharmacotherapy)
Merci
Penumbra
Solitaire
Trevo
3D separator (We are currently enrolled in Therapy trial)
“Solumbra” technique
152. Recommendations for Extracranial CAROTID
Atherosclerotic Disease (Not
Undergoing Revascularization)
Obstructive or nonobstructive with AIS or TIA
aspirin alone (75 to 325 mg daily)
clopidogrel alone (75 mg daily)
aspirin plus extended-release dipyridamole (25 and 200 mg
twice daily, respectively)
Class I, LOE: B
Antiplatelet agents recommended rather than oral
anticoagulation for patients with atherosclerosis of the
extracranial carotid or vertebral arteries with (Class I, LOE:
B) or without (Class I, LOE: C) ischemic symptoms
153. Recommendations for Extracranial CAROTID
Atherosclerotic Disease (Not
Undergoing Revascularization)
If indication for OAC (atrial fibrillation, mechanical
prosthetic heart valve)
Administer vitamin K antagonist (such as warfarin,
dose-adjusted to achieve a target international
normalized ratio [INR] of 2.5 [range 2.0 to 3.0])
(Class IIa, LOE: C)
Unable to take aspirin
Clopidogrel (75 mg daily)
Ticlopidine (250 mg twice daily)
Class IIa, LOE: C
154. Recommendations for Extracranial CAROTID
Atherosclerotic Disease (Not
Undergoing Revascularization)
Anticoagulation with unfractionated heparin or low-molecular-
weight heparinoids is not recommended
for TIA or AIS (Class III, LOE: B)
Clopidogrel in combination with aspirin is not
recommended within 3 months after AIS or TIA (Class
III, LOE: B)
155. Recommendations for Extracranial VERTEBRAL
Atherosclerotic Disease
Vertebral atherosclerosis without AIS or TIA
Aspirin (75 to 325 mg daily)
(Class I, LOE: B)
Vertebral atherosclerosis with AIS or TIA
Aspirin (81 to 325 mg daily)
Aspirin plus extended-release dipyridamole (25 and 200 mg
twice daily, respectively)
Clopidogrel (75 mg daily)
(Class I, LOE: B)
Unable to take aspirin
clopidogrel (75 mg daily) or ticlopidine (250 mg twice daily)
(Class IIa, LOE: C)
156. Extracranial Carotid or Vertebral
Artery Dissection
Dissection associated with AIS or TIA
Anticoagulant (heparin, low-molecular-weight heparin, or
warfarin) for 3-6 months
Platelet inhibitor (aspirin, clopidogrel, or the combination
of extended-release dipyridamole plus aspirin) for 3- 6
months
(Class IIa, LOE: B)
Carotid angioplasty and stenting might be considered
when ischemic symptoms have not responded to
antithrombotic therapy after acute carotid dissection.
(Class IIb,LOE: C)
The safety and effectiveness of pharmacological therapy
to lower blood pressure to the normal range and reduce
arterial wall stress not well established (Class IIb,LOE: C)
157.
158.
159. Hemorrhagic Stroke
Intracerebral Hemorrhage
Ruptured blood vessel in
brain parenchyma
Subarachnoid Hemorrhage
Ruptured blood vessel
(usually aneurysm) on the
surface of the brain
160.
161. Summary of ED Management
for ICH (General)
Rapid neuroimaging with CT/MRI to distinguish AIS from
ICH (Class I; LOA: A)
Treat impending herniation or suspected ICP
Airway protection/hyperventilation
Osmotic agents- Hypertonic saline/mannitol
Control blood pressure
Correct coagulopathy
Treat seizures
Rapid transfer to tertiary care center
Stroke. 2010;41:00-00
162. Summary of ED Management
for ICH (Blood Pressure)
In patients with SBP of 150-220 mmHg, acute
lowering to 140 mm Hg is probably safe (Class IIa;
LOE: B)
Rapid blood pressure lowering in patients with ICH is
safe and does not compromise cerebral blood flow
(http://stroke.ahajournals.org/content/early/2013/02/0
7/STROKEAHA.111.000188.abstract)
Stroke. 2010;41:00-00
163. Summary of ED Management
for ICH (Coagulopathy)
Severe coagulation factor deficiency or thrombocytopenia
Replace deficient factor or platelets (Class I; LOE: C)
Elevated INR related to OAC
Withhold OAC
Administer IV vitamin K and replace vitamin K–dependent
factors to correct the INR (Class I; LOE: C)
PCC reasonable alternative to FFP (Class IIa; LOE: B)
rFVIIa not recommended as a sole agent for OAC reversal in ICH
(Class III; LOE: C)
rFVIIa not recommended in unselected (noncoagulopathic) ICH
due to thromboembolic risk. (Class III; LOE: A)
Stroke. 2010;41:00-00
164. Summary of ED Management
for ICH (Seizures)
Prophylactic anticonvulsant medication should not
be used (Class III; LOE: B)
Clinical seizures should be treated with antiepileptic
drugs (Class I; LOE: A)
Stroke. 2010;41:00-00
165. Summary of ED Management
for ICH
Aggressive full care early after ICH onset and
postponement of new DNR orders until at least the
second full day of hospitalization is recommended
(Class IIa; LOE: B)
Patients with preexisting DNR orders are not
included in this recommendation
Stroke. 2010;41:00-00
166.
167.
168. Summary of ED Management
for Aneurysmal SAH
Worst Headache of Life = noncontrast Head CT; LP if negative
(Class I; LOE: B)
Neuro exam using simple validated scales (Class I; LOE: B)
World Federation of Neurological Surgeons
Hunt /Hess
Control BP with a titratable agent to balance the risk of stroke,
hypertension-related rebleeding, and maintenance of cerebral
perfusion pressure (Class I; LOE: B)
Goal decrease SBP <160 mm Hg is reasonable (Class IIa; LOE: C)
Maintain MAP < 110, avoid hypotension (low quality evidence;
strong rec)
Stroke. 2012;43:1711-1737.
Neurocrit Care (2011) 15:211–240
169. Summary of ED Management
for Aneurysmal SAH
Transfer to high-volume centers with experienced
cerebrovascular surgeons, endovascular specialists, and
multidisciplinary neuro-intensive care services (Class I; LOE: B)
Seizure prophylaxis
Consider short course (very low qual; weak rec)(Class IIb; LOE: B)
Phenytoin should NOT be used (low qual; strong rec)
Use isotonic crystalloids (mod qual; weak rec)
Avoid hypoglycemia (high qual; strong rec)(Class IIb; LOE: B)
Maintain glucose < 200mg/dL (mod qual; strong rec)
Stroke. 2012;43:1711-1737.
Neurocrit Care (2011) 15:211–240
177. Atrial Fibrillation: Clinical Problems
Embolism and stroke (presumably due to LA clot)
Acute hospitalization with onset of symptoms
Anticoagulation, especially in older patients (> 75 yr.)
Congestive heart failure
– Loss of AV synchrony
– Loss of atrial “kick”
– Rate-related cardiomyopathy due to rapid
ventricular response
Rate-related atrial myopathy and dilatation
178. Atrial Fibrillation
Atrial fibrillation (AF) is not one disease
process
Currently there is no unitary hypothesis on
the mechanism of AF
AF is progressive
There is no treatment that is 100%
effective in the prevention of AF
179. Interaction of LV, LA and Afib
Not one disease process
Afib
LV LA
Rate-related
Changes
HTN
CHF
Sleep
Apnea Structural
Changes
180. Forms of AF
Paroxysmal
Paroxysmal lasting less than 48 hours
Persistent
An episode of AF lasting greater than 48 hours,
which can still be CV to SR
Permanent
Inability of pharmacologic or non-pharmacologic
methods to restore SR
182. Atrial Fibrillation
• The genesis of AF appears to originate in the atrial
muscular sleeves surrounding the PVs
• PAC’s and runs of AT originating in these sleeves
result in tachycardia-induced electrical remodeling of
the PV-LA junction
• The architecture of the PV-LA musculature and
remodeling allows for localized reentry and
fibrillatory conduction resulting in AF
• Continuation of AF leads to remodeling of the LA
(particularly the posterior wall) and perpetuation and
maintenance of AF
183. Atrial Fibrillation
• The unique electrophysiological properties of the PV
cardiomyocytes may account for their central role in
AF genesis
• PV cardiomyocytes appear to be susceptible to
calcium mediated DAD’s and triggered activity
resulting in PAC’s and AT
• Triggered activity in PV’s has been shown to be
induced by stretch and sympathetic and
parasympathetic nerve stimulation
• Studies have shown high density autonomic nerve
innervation at ostia of PV and posterior wall of LA
• Autonomic nerve denervation may be a important
component of AF ablation
188. EMBRACE Conclusions
1 in 6 patients aged ≥55 years with ‘cryptogenic’ stroke or
TIA has paroxysmal AF
– 1 in 5 patients over age 75 years
1 or 2 Holter monitors post-stroke/TIA is insufficient to
exclude paroxysmal AF
Prolonged continuous monitoring for a target of 30 days –
is feasible
– significantly more effective for paroxysmal AF detection –
has an incremental yield over 30 days
– resulted in a significant increase in anticoagulant use
189.
190. Atrial Fibrillation
Clinical Problems
Acute hospitalization with onset of symptoms
Embolism and stroke (presumably due to LA clot)
Anticoagulation, especially in older patients (>75 yr.)
Congestive heart failure
– Loss of AV synchrony
– Rate-related cardiomyopathy due to rapid ventricular response
Rate-related atrial myopathy and dilatation
Chronic symptoms and reduced sense of well-being
191. Implications of Varying Levels
of AF on Stroke Risk
Methods:
• Analysis of 568 patients with an IPG and a history
of AF
• Three AF groups were considered: patients with <
5-minutes AF on 1 day (AF-free); patients with >
5-minutes AF on 1 day but
< 24 hours (AF-5 minutes); patients with AF
episodes > 24 hours (AF-24 hours)
Results/Conclusions:
• “In patients with recurrent AF episodes, risk
stratification for thromboembolic events can be
improved by combining CHADS2 score with AF
presence/duration.”
5 Botto G, et al. J Cardiovasc Electrophysiol. 2009;20:241-248.
Risk of Thromboembolic Events
192. Background
Identification of atrial fibrillation (AF) is a key goal in secondary stroke
prevention
Anticoagulant therapy is highly beneficial for stroke prevention in
individuals with AF (paroxysmal or permanent)
– reduces stroke risk by 64%; reduces death by 25%
– ≈40% additional stroke risk reduction compared to antiplatelet therapy
Paroxysmal AF can be difficult to detect and likely underdiagnosed in
patients with stroke/TIA
Efforts to improve AF detection are needed and could lead to more strokes
prevented
197. EMBRACE Patient Population
Age ≥55 years without previously documented AF
Acute embolic arterial ischemic stroke (confirmed by neuroimaging) or
TIA, of undetermined etiology (TOAST classification), occurring
within the previous 6 months
Negative stroke work-up:
– 12-leadECG(s)
– Holter monitor
– vascular imaging with CTA or MRA (carotid ultrasound acceptable for
anterior circulation events)
– echocardiography(2DorTEE)
• Exclusions: most responsible etiology of large vessel disease, small
vessel disease, or other determined etiology
209. New Modes and Models of care:
Readmissions, Observation and
Transition Strategies
Jennifer Jackson, MD
Jennifer Rodgers, APRN
Robyn Chadwick, LSCSW
210. New England Journal 2009
“75% of readmissions are preventable”
Stephen Jencks
Medicare claims 2003-04
19.6% readmitted within 30 days
34% readmitted within 90 days
211. A Sobering Statistic
67% of medical patients &
52% of surgical patients
were back in the hospital
or dead
within one year
Most patients are high risk
212. Most Common Discharge Diagnosis
that are Readmitted
Medical 21%
• Heart Failure
• Pneumonia
• COPD
• Psychosis
• GI problems
Surgical 15.6%
• Cardiac stent
• Hip or Knee
• Other vascular
• Major bowel
• Other hip/femur
213. Opportunities?
Half the medical bounce backs had NO follow-up
between discharge and readmission
If you came back after a surgical procedure, 70%
of the time it was for a medical reason
60% of all prescriptions are NEVER filled
214. Centers for Medicare Response
$17.4 billion dollars in unplanned rehospitalizations
• ACA 3025: Penalties for high readmission rates
• Starting in FY 2013, penalties for hospitals with “higher
than expected” readmission rates within 30 days of
discharge for heart attack, heart failure, and pneumonia.
• Maximum penalty: 1% of Medicare payments in FY 2013,
2% in 2014, 3% in 2015.
• Secretary is to increase the number of included discharge
conditions (hint: COPD is next)
215. Centers for Medicare Response
“These things matter to hospitals,
not to physicians”
Physician specific penalties for readmissions
216. Breaking Down the Silos
“Make hospitals responsible for the factors
outside the hospital that cause readmission”
217. Why do people come back?
Medications are confusing Follow-up not timely
Patient chronic clinical factors (chronic conditions)
Patient acute Call clinical 911 when factors they get (into DRG)
trouble
Social factors (literacy, social support, money,
Missed opportunity for palliative care or hospice
transportation, housing)
Transition planning and execution (process design,
medication reconciliation, follow-up contact)
Emergency care issues (lack of alternatives to ER,
limited dispositional choices)
Don’t understand instructions
No transportation to pharmacy/provider
Can’t afford medications
Resume previous lifestyle habits
Poor health care literacy
Can’t get in for follow-up
Discharge is a mess
218. Readmissions Reasons
the low hanging fruit?
1. Did not fill prescriptions at discharge
2. Did not understand how to correctly take
medications (took new AND old)
3. No follow up with PCP or specialist within 7
days post discharge
4. Einstein Hospital, Philadelphia, PA study
219. “The evidence for preventability rests on
successful interventions
not on evidence of defective care”
There are opportunities
We really could do a better job
220. Interventions to Reduce
30-Day Readmissions
Pre-discharge
• Patient education
• Discharge planning
• Medication reconciliation
• Appointment scheduled
before discharge
Post-discharge
• Timely follow-up
• Timely PCP communication
• Follow-up telephone call
• Patient hotline
• Home visit
Bridging the Transition
•Transition coach
•Patient centered discharge instruction
•Provider continuity
Annals Internal Medicine 2011 PMID 22007045
221. Hospital Discharge Program
• 749 hospitalized patients
• Nurse discharge advocate: follow-up
appointments, confirmed discharge
medications, individualized discharge
instructions, connected to PCP
• Pharmacist called 2-4 days after discharge
• Outcome: decreased hospitalization & ED
visits
Ann Intern Med 2009 PMID 19189907
222. Care Transitions Intervention
(Coaching)
• 750 patients
• Transitions coach and tools to promote
communication
• 4 pillars:
– Medication management
– Patient owner of records
– Timely follow-up
– Red flag symptoms with response
• Outcome: decreased 30 day readmission and at
180 days
Arch Intern Med 2006 PMID 17000937
223. Transitions of Heart Failure Patients
• 239 patients
• 3 months APRN discharge and home follow-up
• Outcome: increased time to next admission,
reduced total number of hospitalizations,
decreased overall cost
J AM Geriatr Soc 2004 PMID 15086645
224. The Via Christi
Transitional Care Programs
• Improve Access to Care
• Focus on Quality of Life
• Focus on Connection to Care
• Serve Vulnerable Patient Populations
225. Post-discharge
Timely follow-up
Timely PCP
communication
Follow-up
telephone call
Patient hotline
Home visit
Via Christi Heart Failure
Disease Management Program
• Joint Commission certified since 2003
• Target high risk heart failure patients
• Focus on quality of life
• Follow 30 day readmission data
• Three goals:
– Patient empowerment in disease process
– Med and device titration
– Collaboration with PC/C
226. Heart Failure Readmissions
30%
25%
20%
15%
10%
5%
0%
30 Day Readmissions
National Via Christi Heart Failure
227. Via Christi Community Cares
• High risk pulmonary patients
• APRN home visits
• Crisis line/after hours care
• Connect to meds, supplies, DME
• Emergency kit in home
Post-discharge
Timely follow-up
Timely PCP
communication
Follow-up
telephone call
Patient hotline
Home visit
228. 400
350
300
250
200
150
100
50
0
Community Cares Program Patient Summary
12 months before joining program
All patients to date = 55 patients
Over 550 encounters
ED Visits Inpatient Admissions
229. 60
50
40
30
20
10
0
Community Cares Program Patient Summary
30 days before and after joining program
To Date N = 55 patients
ED visits reduced by 73%
Admits reduced by 93%
30 Days Before CCP 30 Days After CCP
ED Visits Inpatient Admissions
230. Via Christi Transitional Clinic
• Discharge clinic—bridge to continuity provider
• Connect to medications, DME, services
• Continue insurance applications, disability
process
• Timely follow-up
• Patient navigation
Bridging the Transition
Transition coach
Patient centered discharge instruction
Provider continuity
232. 500
450
400
350
300
250
200
150
100
50
0
Transitions Clinic Patient Summary
12 months before joining program
Total to Date = 155 patients
Over 650+ encounters
ED Visits OBS Inpatient Admissions
233. 200
180
160
140
120
100
80
60
40
20
0
Transitions Clinic Patient Summary
30 days before and after joining program
Total to Date N = 155
ED reduced by 82%
Admits reduced by 81%
30 Days Before TOC 30 Days After TOC
ED Visits OBS Inpatient Admissions
234. +
Heart Disease in Women - An Update
Via Christi Cardiovascular Symposium
Shilpa Kshatriya, MD, FACC
10/24/14
236. +
Prevalence of CAD
CAD leading cause of death in men and women in the US
More women than men die of CAD (455,000 vs. 410,000)
1 in 3 women die from heart disease
1 death a minute
From 1998 to 2008, the rate of death attributable to CAD declined 30.6%, but the
rates are increasing in young women (<55 years)
The average age at first myocardial infarction (MI) is 64.5 years for men and 70.3
years for women. The incidence of CAD in women lags behind men by 10 years
and by 20 years for more serious clinical events such as MI and sudden death
Continued increase with aging population and with epidemics of obesity, diabetes
and metabolic syndrome
2014 Heart Disease and Stroke Statistics
Centers for Disease Control and Prevention. State-Specific Mortality from Sudden Cardiac Death—United States, 1999.
237. + Prevalence of CV disease in adults by age and sex (National
Health and Nutrition Examination Survery: 2007-2010)
238. +
Age-Adjusted Death Rates In Females
National Center for Health Statistics and National Heart, Lung, and Blood Institute.
239. + Prevalence of Heart Failure by Age and Sex:
NHANES: 2007 – 2010)
243. + Worse Consequences of CAD
Among individuals with premature MI (under age 50), women
experience a 2-fold higher mortality rate after acute MI
compared to men
Among older individuals (over the age of 65), women are more
likely to die within the first year after MI.
In individuals 45 to 64 years of age, women are more likely
than men to have heart failure within 5 years of MI.
Higher rates of angina
Greater proportion of women die of sudden cardiac death
before their arrival at a hospital (52%) contrasted with 42% of
men
Vaccarino V et al. Sex- based differences in early mortality after myocardial infarction. National Registry of Myocardial Infarction 2
Participants. N Engl J Med 1999;341:217–25.
Hemingway H et al.Prevalence of angina in women versus men: a systematic review and meta-analysis of international varia- tions
across 31 countries. Circulation 2008;117:1526–36.
Murphy SL. Death: final data for 1998. Natl Vital Stat Rep 2000;48: 1–105.
244. +C ardiovascular Disease Mortality Trends
National Center for Health Statistics and National Heart, Lung, and Blood Institute.
245. +
Greater Health Care Costs
1) more frequent diagnoses of angina, office visits, and
hospitalizations
2) greater myocardial infarction (MI) mortality
3) greater rates of heart failure hospitalization as compared with
men
Shaw LJ, Sharaf BL, Johnson BD, et al. The economic burden of angina in women with
suspected ischemic heart disease: results from the National Institutes of Health–National
Heart, Lung, and Blood Institute-Sponsored Women’s Ischemia Syndrome Evaluation (WISE).
Circulation 2006;114:894–904.
246. +
Three Paradoxes
1. Women have a higher prevalence of angina compared to
men, yet have an overall lower prevalence of atherosclerosis
and obstructive coronary artery disease (CAD).
2. Symptomatic women undergoing coronary angiography have
less extensive and severe CAD, despite being older with a
greater risk factor burden, compared to men.
3. Despite relatively less CAD, women have a more adverse
prognosis compared to men.
Merz CB, Shaw L et al. Ischemic heart disease in women: insights from the NHLBI-sponsored Women’s Ischemic Syndrome Evaluation (WISE) study.
Part II: sex differences in presentation diagnosis, and outcome with regard to sex-based pathophysiology of atherosclerosis, macro and microvascular
CAD. J Am Coll Cardiol 2006;47
247. +
Female Specific IHD
Abnormal coronary reactivity
Microvascular dysfunction
Plaque erosion/distal microembolization
Shaw LJ, Bairey Merz CN, et al., for the WISE Investigators. Ischemic heart disease in women: insights from the NHLBI- sponsored Women’s Ischemia
Syndrome Evaluation (WISE) study. Part I: sex differences in traditional and novel risk factors, symptom evaluation and gender-optimized diagnostic
strategies. J Am Coll Cardiol 2006;47:S4 –20.
Von Mering GO et al, for the National Heart, Lung, and Blood Institute. Abnormal coronary vasomotion as a prognostic indicator of cardiovascular events
in women: results from the National Heart, Lung, and Blood Institute-Sponsored Women’s Ischemia Syndrome Evaluation (WISE). Circulation 2004;109:
722–5.
251. +
Prognosis
Greater mortality in women compared to men
National Registry of Myocardial Infarction-2 (NRMI-
2) analyzed data from 380,000 patients and found
that in younger patients < 50 years, mortality in
women was more than twice that of men
OBSTRUCTIVE CAD- 2 fold greater risk of in-hospital
mortality than nonobstructive CAD.
Vaccarino V, et al. Sex-based differences in early mortality after myocardial infarction. National Registry of Myocardial
Infarction 2 Participants. N Engl J Med 1999;341:217–25.
Shaw LJ,, et al. Impact of ethnicity and gender differences on angiographic coronary artery disease prevalence and in-hospital
mortality in the American College of Cardiology– National Cardiovascular Data Registry (ACC-NCDR).
Circulation 2008;117:1787– 801.
252. + Prognosis of Nonobstructive CAD
o Not benign
o Worse prognosis
o 30% of women with chest pain, normal angiograms and endothelial
dysfunction developed obstructive CAD during a 10 year follow-up.
o For women presenting with ACS/ST- segment elevation myocardial
infarction (STEMI), 10% to 25% of women as compared with 6% to 10%
of men have no obstructive CAD---amounts to 60,000 to 150, 000
women
o Often treated with reassurance, sedative-hypnotics and repeat
hospitalisation
Kemp HG, et al. Seven year survival of patients with normal or near normal coronary arteriograms: a CASS registry study. J Am Coll Cardiol
1986;7:479 – 83
Lichtlen PR, et al. Long-term prognosis of patients with anginalike chest pain and normal coronary angiographic findings. J Am Coll Cardiol
1995;25:1013– 8.
253. +
Nonobstructive CAD = CV events
A Report From the Women’s Ischemia Syndrome Evaluation Study and the
St James Women Take Heart Project
Arch Intern Med. 2009;169(9):843-850
254. +
Prognosis
Among those undergoing coronary angiography, as many as
50% of women do not have obstructive CAD.
Women report more angina despite lower rates of obstructive
CAD
Women’s Ischemia Syndrome Evaluation -46% of women with
chest pain and negative coronary angiograms had continued
anginal symptoms at 5 year follow-up
Data from the Women’s Health Initiative document that women
with nonspecific chest pain have a 2-fold greater risk for
nonfatal MI
Sharaf BL,, et al. Detailed angiographic analysis of women with suspected ischemic chest pain (pilot phase data from the NHLBI-sponsored
Women’s Ischemia Syndrome Evaluation [WISE] Study Angiographic Core Laboratory). Am J Cardiol 2001;87:937–41.
Merz NB, et al. Diagnostic, prognostic, and cost assessment of coronary artery disease in women. Am J Manag Care 2001;7:959–65.
Robinson JG, et al. Cardiovascular risk in women with non-specific chest pain (from the Women’s Health Initiative Hormone Trials). Am J
Cardiol 2008;102:693–9.
255. +
Dallas Heart Study
Angina was not related to atherosclerosis measured by Coronary
Calcium score but was related to risk factors---central obesity,
insulin resistance, serum inflammatory markers and reduced aortic
compliance
64% atherosclerosis without angina
7% symptomatic atherosclerosis
29% angina in the absence of atherosclerosis
Therefore 1/3 of women have signs and symptoms of myocardial
ischemia without evident CAD, out of 6 million women in US with
CAD, 2 to 3 million have signs and symptoms of ischemic heart
disease in the absence of CAD
Banks et al. JACC Imaging 2011
258. +
Risk Assessment
Framingham risk score underestimates risk in women
FRS classifies > 90% women as low risk, with very few
assigned as high risk before the age of 70
When compared with the FRS, use of the Reynolds score
resulted in risk reclassification in 40% of intermediate FRS
women
Ridker PM, Buring JE, Rifai N, Cook NR. Development and validation of improved algorithms for the assessment of global cardiovascular risk in women: the
Reynolds Risk Score. JAMA 2007;297:611–9.
Wenger NK. The Reynolds Risk Score: improved accuracy for cardiovascular risk prediction in women? Nat Clin Pract Cardiovasc Med 2007;4:366–7.
Michos ED, et al. Framingham risk equation underestimates subclinical atherosclerosis risk in asymptomatic women. Atherosclerosis 2006;184:201–6.
259. +
Risk Scores
Framingham Risk Score
Age
Gender
Smoking history
SBP
TCHOL
HDL
Reynolds Risk Score
Age
Gender
Smoking History
SBP
TCHOL
HDL
hsCRP
FH of MI < 60 years
cvdrisk.nhlbi.nih.gov/ www.reynoldsriskscore.org/
260. +
Risk Assessment- Calcium Score
Calcium score improves risk prediction in women.
In MESA (Multi-Ethnic Study of Atherosclerosis), 3,601 women
were studied, and 90% were classified as low risk.
Prevalence of any coronary calcium was associated with a 6-
fold increased risk of CAD, adjusted for age, ethnicity, body
mass index, low-density lipoprotein, high blood pressure,
smoking, estrogen, and statin therapy.
A calcium score of > 300 was associated with an 8.6%
absolute risk of CAD.
The presence of coronary calcium therefore redefined a group
of women improperly labeled as low risk by Framingham
criteria
Lakoski SG, et al. Coronary artery calcium scores and risk for cardiovascular events in women classified as “low risk” based on Framingham risk score:
the Multi- Ethnic Study of Atherosclerosis (MESA). Arch Intern Med 2007; 167:2437– 42.
262. +
Lakoski SG, et al. Coronary artery calcium scores and risk for cardiovascular events in women classified as “low risk” based on
Framingham risk score: the Multi- Ethnic Study of Atherosclerosis (MESA). Arch Intern Med 2007; 167:2437– 42.
264. + The “Effectiveness-Based Guidelines for the
Prevention of Coronary Artery Disease in Women—
2011 Update”
1. High Risk
2. At risk
3. Optimal risk
Circulation. 2011 March 22; 123(11): 1243–1262
266. +
Risk Factors
Premature paternal history of a heart attack has been shown to approximately double the
risk of a heart attack in men and increase the risk in women by ≈70% .
Hypertension is more prevalent in women, particularly older women. Women with
hypertension have a higher risk of developing congestive heart failure than men do.
The age-adjusted prevalence of hypertension (both diagnosed and undiagnosed) in 2003
to 2006 was 75% for older women and 65% for older men on the basis of data from
NHANES/NCHS
After the fifth decade of life, women have higher cholesterol levels than men do.
When women with 2 or more risk factors were compared to women with no risk factors,
those without risk factors had a substantially lower lifetime risk of CAD (8.2% vs. 50.2%)
Lloyd-Jones DM, et al. Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and
offspring . JAMA . 2004;291:2204–2211 .
Scheuner MT, et al. Relation of familial patterns of coronary heart disease, stroke, and diabetes to subclinical atherosclerosis: the Multi-Ethnic Study of
Atherosclerosis. Genet Med 2008;10:879–87.
Centers for Disease Control and Prevention. Health, United States, 2009: With Special Feature on Medical Technology. 2010.
Levy D, et al.. The progression from hypertension to congestive heart failure. JAMA 1996;275:1557–62
267. + Prevalence of high blood pressure in adults ≥20 years of age by
age and sex (National Health and Nutrition Examination Survey:
2007–2010)
268. +
Risk Factors
The presence of diabetes is a relatively greater risk factor for
CAD in women versus men, increasing a woman’s risk of CAD
by 3- to 7-fold, with only a 2- to 3-fold increase in diabetic men.
Women with diabetes have a greater than 3-fold increase in
CAD risk than nondiabetic women do.
Huxley R, et al. Excess risk of fatal coronary heart disease associated with diabetes in men and women: meta-analysis of 37 prospective
cohort studies. BMJ 2006;332:73–8.
270. +
Risk Factors
Men were more likely to have engaged in moderate to vigorous
PA ≥3 times per week than women (60 .3% versus 53 .1%,
respectively)
Lack of physical fitness is a predictor of mortality.
In the St. James Women Take Heart Project, asymptomatic
women who were unable to achieve 5 metabolic equivalents
(MET) on a Bruce protocol have a 3-fold increased risk of death
compared with women who achieved >8 METS, even after
controlling for traditional risk factors .
Gulati M, Pandey DK, Amsdorf MF, et al. Exercise capacity and the risk of death in women: the St. James Women Take Heart Project.
Circulation 2003;108:1554–9.
272. +
Novel Risk Factors
Traditional risk factors and Framingham risk score (FRS)
underestimate CHD risk
Women have a higher CRP level than men
PCOS – 1.70
Pre-eclampsia – 2.0
Gestational DM- 1.71
273. + Pre-eclampsia and risk of cardiovascular disease and
cancer in later life: systematic review and meta-analysis
Bellamy et al. BMJ 2007;335:974.
RR of HTN- 3.70
Ischemic Heart Disease- 2.16
Stroke- 1.81
Venous Thromboembolism- 1.79
All-cause mortality- 1.49
No increased risk of cancer
A history of pre-eclampsia should be obtained when assessing CV
risk
274. P+re- eclampsia and risk of cardiovascular disease and cancer in later
life: systematic review and meta-analysis
Bellamy et al. BMJ 2007;335:974.
275. +
Novel Risk Factors
Autoimmune diseases e.g. SLE, RA
Breast Cancer and therapy
Depression
276. +
Traditional Framingham Risk Factors Do Not
Fully Explain Risk of Atherosclerosis in SLE
Canadian cohort of 296 patients
Even after controlling for age, sex, cholesterol, HTN, DM,
tobacco use
10 x Increased risk for nonfatal MI
17 x Increased risk for death due to CAD
8 x Increased Risk for Stroke
Esdaile JM,et al. Traditional Framingham risk factors fail to fully account for accelerated atherosclerosis in systemic lupus erythematosus.
Arthritis Rheum 2001.
277. A+ge -specific Incidence Rates of Myocardial Infarction and Angina
in Women with Systemic Lupus Erythematosus: Comparison with
the Framingham Study
Manzi et al. also found that women with SLE in the 35–44-year age
group were over 50-times more likely to have a MI than women of a
similar age in the Framingham Offspring Study
1. Older age at lupus diagnosis
2. Longer lupus disease duration
3. Longer duration of corticosteroid use
4. Hypercholesterolemia
5. Postmenopausal status
MORE COMMON
IN THOSE WITH
LUPUS WHO HAD
A CARDIAC
EVENT
Am J Epidemiol 1997;145:408-15
280. +
Diagnosis of Myocardial Ischemia
Duke Treadmill Score- is particularly useful in women and
performs better in women than in men for predicting significant
CAD
DTS = Exercise time – (5 x ST segment deviation) – (4 x treadmill
angina)
0 - no angina during exercise,
1- non limiting angina during exercise
2 - exercise-limiting angina
Low risk (DTS score of ≥ 5)
Moderate risk (DTS score between 5 and - 11)
High risk (DTS score > - 11)
Alexander KP, Shaw LJ et al. Value of exercise treadmill testing in women. J Am Coll Cardiol
1998;32:1657–64.
282. Role of Noninvasive Testing in the Clinical Evaluation of
Women With Suspected Coronary Artery Disease.
+
Mieres et al.Circulation. 2005;111:682-696
Algorithm for evaluation of symptomatic women using exercise ECG or cardiac
imaging.
283. + Assessment of Microvascular
Dysfunction
Invasive Coronary Reactivity
Cardiac MR perfusion imaging
Myocardial Blood Flow reserve by PET
285. +
Diagnosis Of Ischemia
Stress Cardiac Magnetic Resonance (CMR)
A recent study of predominantly female patients with chest pain and
nonobstructive CAD who underwent adenosine CMR found that
subendocardial ischemia was frequently present when compared with
images of control subjects
In a small substudy from the WISE cohort, women with nonobstructive
CAD with an abnormal stress-induced CMR had an increase in
adverse cardiovascular events
Panting JR,, et al. Abnormal subendocardial perfusion in cardiac syndrome X detected by cardiovascular magnetic resonance imaging. N Engl J
Med 2002;346:1948–53
Johnson BD, et al. Prognosis in women with myocardial ischemia in the absence of obstructive coronary disease: results from the National
Institutes of Health National Heart, Lung, and Blood Institute Sponsored Women’s Ischemia Syndrome Evaluation (WISE). Circulation
2004;109:2993–9.
286. +
N Engl J Med, Vol. 346, No. 25 · June 20, 2002
287. + Invasive Coronary Reactivity Testing
Gold standard to diagnose microvascular dysfunction
Angina + abnormal stress test + “normal coronaries” or nonobstructive
CAD ( < 50%)
Nonendothelial-dependent microvascular function-intracoronary
incremental doses of adenosine (18ug, 18ug, 36ug) to create maximal
hyperemia and CORONARY FLOW RESERVE obtained ( ratio of peak
velocity/baseline velocity). A CFR ≤ 2.5 is ABNORMAL.
Endothelial dependent microvascular and macrovascular function-incremental
doses of intracoronary acetyl choline (0.182 and 18.2ug/ml).
Normal microvascular function- 50% increase in coronary blood flow.
Normal macrovascular function is coronary artery dilation > 5%.
Nonendothelial dependent macrovascular function-intracoronary
nitroglycerin (200ug) injected and baseline and peak velocities obtained.
Normal response - > 20% increase in diameter.
Am Coll Cardiol Intv 2012;5:646–53
289. + Management of Obstructive CAD
Why is mortality due to ACS higher in women?
Women treated less aggressively than men
In the CRUSADE initiative, women were less likely to receive
heparin and glycoprotein (GP) IIb/IIIa inhibitors and were less
likely to undergo cardiac catheterization than men were.
Women with ACS have also been shown to be less likely to
receive early aspirin, beta-blockers, and timely reperfusion
Higher rates of bleeding
Women have a higher risk of morbidity and mortality and they
experience less relief from angina than do men after CABG
Cardiac rehabilitation after MI is underused in women
Jneid H, et al, for the Get With the Guidelines Steering Committee and Investigators. Sex differences in medical care and early
death after acute myocardial infarction. Circulation 2008;118:2803–10.
Blomkalns AL, et al, for the CRUSADE Investigators. Gender disparities in the diagnosis and treatment of non ST-segment
elevation acute coronary syndromes: large-scale observations from the CRUSADE National Quality Improvement Initiative. J
Am Coll Cardiol 2005;45:832–7.
Witt BJ, et al. Cardiac rehabilitation after myocardial infarction in the community. J Am Coll Cardiol 2004;44: 988–96.
290. +
Management of Obstructive CAD
A meta-analysis of randomized controlled trials of ACS showed
that an invasive strategy was more beneficial in women with
positive biomarkers in contrast to women with negative
biomarkers; such a difference was not seen in men
Women have a greater mortality after percutaneous coronary
intervention (PCI) for ST-segment elevation and non ST-segment
elevation MI than men
O’Donoghue M, Boden WE, Braunwald E, et al. Early invasive vs. conservative treatment strategies in women and men with unstable angina and
noneST-segment elevation myocardial infarction: a meta-analysis. JAMA 2008;300:71–80.
Lansky AJ. Outcomes of percutaneous and surgical revascularization in women. Prog Cardiovasc Dis 2004,46:305–19.
291. M+a nagement of Nonobstructive CAD
Patients with unstable angina and no critical coronary
obstruction have a 2% risk of death and MI at 30 days after MI
Improve endothelial function –statins, ACE-I, beta blockers
Calcium channel blockers reduce coronary flow reserve and
may not improve symptoms
Exercise training improves symptoms
Randomized trial data lacking
Diver DJ,, et al. Clinical and arteriographic characterization of patients with unstable angina without critical coronary arterial narrowing (from the TIMI-IIIA Trial). Am J Cardiol 1994;74:531–7.
izzi C, et al. Angiotensin-converting enzyme inhibitors and 3-hydroxy-3-methylglutaryl coenzyme A reductase in cardiac Syndrome X: role of superoxide dismutase activity. Circulation
2004;109:53–8.
Danao!glu Z, et al. Effect of statin therapy added to ACE-inhibitors on blood pressure control and endothelial functions in normolipidemic hypertensive patients. Anadolu Kardiyol Derg
2003;3:331–7.
Kayikçio!glu M, et al. Benefits of statin treatment in cardiac syndrome-X1. Eur Heart J 2003;24:1999–2005.
Eriksson BE, et al. Physical training in Syndrome X: physical training counteracts deconditioning and pain in Syndrome X. J Am Coll Cardiol 2000;36:1619–25.
292. R+an olazine Improves Angina in Women With Evidence of
Myocardial Ischemia But No Obstructive Coronary Artery
Disease
A randomized, double-blind, placebo-controlled, crossover trial was
conducted in 20 women with angina, no obstructive CAD, and >10%
ischemic myocardium on adenosine stress cardiac magnetic resonance
(CMR) imaging.
Participants were assigned to ranolazine or placebo for 4 weeks
separated by a 2-week washout.
The Seattle Angina Questionnaire and CMR were evaluated after each
treatment. Invasive coronary flow reserve (CFR) was available in patients
who underwent clinically indicated coronary reactivity testing. CMR data
analysis included the percentage of ischemic myocardium and quantitative
myocardial perfusion reserve index (MPRI).
R E S U L T S : The mean age of subjects was 57 ± 11 years. Compared
with placebo, patients on ranolazine had significantly higher (better)
Seattle Angina Questionnaire scores. There was a trend toward a higher
(better) CMR mid-ventricular MPRI (2.4 [2.0 minimum, 2.8 maximum] vs.
2.1 [1.7 minimum, 2.5 maximum], p = 0.074) on ranolazine. Among
women with coronary reactivity testing (n =13), those with CFR ≤3.0 had a
significantly improved MPRI on ranolazine versus placebo compared to
women with CFR >3.0
293. R+an olazine Improves Angina in Women With Evidence of
Myocardial Ischemia But No Obstructive Coronary Artery
Disease
J Am Coll Cardiol Img 2011;4:514–22
294. +
Summary
Ischemic Heart Disease is a more appropriate term to describe the
spectrum of CAD in women
Despite lower prevalence compared to men, women have higher
mortality, hospitalisation rate and are more likely to have
persistent symptoms.
Both traditional risk factors and novel risk factors contribute to risk
Framingham Risk Score may underestimate risk
Nonobstructive CAD is not a benign diagnosis
Guideline-based therapy underutilised
Future investigation should be tailored to identifying diagnostic
and therapeutic strategies to improve outcomes in women