The document discusses screening patients for cardiovascular risk factors and disease. It outlines various risk assessment tools like the Framingham Risk Score and SCORE that estimate risk based on factors like age, cholesterol levels, blood pressure, smoking status. It discusses limitations of risk factor-based screening and emphasizes the importance of directly measuring subclinical disease using tests like coronary artery calcium scoring and carotid intima-media thickness to identify vulnerable patients. The document advocates screening for and treating the underlying atherosclerotic disease rather than just risk factors to improve prevention outcomes.
Arterial health throughout cancer treatment and exercise rehabilitation in wo...
Cardiac risk evaluation: searching for the vulnerable patient
1. Dr. Felix Nunura
Heart Institute of the Caribbean (HIC)
UTJ Adjunct Associate Professor of Medicine
CARDIAC RISK EVALUATION:
Searching for the vulnerable
patient
September, 2012
4. What do you think about this
patient ?
23 points,
22 % CV Risk
5. What do you think about this patient..?
18 points,
> 30 % CV Risk
6. The risk of develop CV disease ( CHD or Stroke) in
the next 10 years in percent (%) can be calculated
with the help of the Framingham Risk Score
Gender, Age, Total-C , HDL-C, SBP, Smoking status
7. Systematic COronary Risk Evaluation (SCORE): based on gender,
age, total cholesterol, systolic blood pressure and smoking status.
Roques F, Michel P, Goldstone AR, Nashef SA. The logistic EuroSCORE.
Eur Heart J. 2003 May;24(9):882-3
8. Effects of any treatment (to lower
cholesterol / lower blood pressure) that
reduced the risk of CVD in 50 %
100
ptes
With
20%
CV
Risk 20
80
Treatment
10
80
10
Will develop CHD or Stroke in the
next 10 years
Will not develop CHD or
Stroke in the next 10 years
9. 1994 4S 2002 PROSPER
1995 WOSCOPS 2002 ALLHAT-LLA
1996 CARE 2002 ASCOT-LLA
1998 AFCAPS/TEXCAPS 2004 PROVE-IT
1998 LIPID 2004 A to Z
2001 MIRACL 2005 TNT
2002 HPS 2005 IDEAL
2008 JUPITER
Study populations:
Primary prevention
Acute coronary syndromes (Secondary prevention)
Chronic Coronary heart disease (Secondary prevention)
*Trials with clinical outcomes
HMG-CoA Reductase Inhibitor:STATINSHMG-CoA Reductase Inhibitor:STATINS
Chronological Order of Event Driven TrialsChronological Order of Event Driven Trials
10. Efficacy of antihypertensive treatmentEfficacy of antihypertensive treatment: Duration and homogeneity of
the efficacy of antihypertensive drugs are currently quantified by
computation of the smoothness index (SI) from ambulatory blood
pressure monitoring (ABPM) recordings.
The smoothness index (SI) identifies
the occurrence of a balanced 24 h
blood pressure reduction with
treatment and correlates with the
favourable effects of treatment on left
ventricular hypertrophy better than
the commonly used trough : peak
ratio.
According to the standard definition,
the SI is calculated as the ratio
between the mean hourly reductions
and the standard deviation of these
reductions. (American Journal of
Hypertension 2005; 18, 24A )
11. General Cardiovascular Risk
Profile for Use in Primary Care
The Framingham Heart Study
Ralph B. D’Agostino, Sr, PhD; Ramachandran S. Vasan, MD;
Michael J. Pencina, PhD; Philip A. Wolf, MD; Mark Cobain,
PhD; Joseph M. Massaro, PhD; William B. Kannel, MD
Circulation. 2008;117:743-753.
12. Background
• Framingham risk score effective, but only predicts
CHD risk .
• CV diseases share common risk factors
• …a way to predict risk for all CVD events
JAMA. 2007;298(7):776-785
Circulation. 2008;117:743-753.
13. Sex
male (m) or female
(f) f
Age years 30
Systolic Blood Pressure mmHg 125.0
Treatment for Hypertension yes (y) or no (n) n
Smoking yes (y) or no (n) n
Diabetes yes (y) or no (n) n
Body Mass Index kg/m² 22.5
Your 10-Year Risk
(The risk score shown is derived on the
basis of an equation. Other print products,
use a point-based system to calculate a
risk score that approximates the equation-
based one.)
1.1%
Sex
male (m) or female
(f) f
Age years 24
Systolic Blood Pressure mmHg 125.0
Treatment for Hypertension yes (y) or no (n) n
Smoking yes (y) or no (n) n
Diabetes yes (y) or no (n) n
HDL mg/dL 45
Total Cholesterol mg/dL 180
Your 10-Year Risk
(The risk score shown is derived on
the basis of an equation. Other print
products, use a point-based system to
calculate a risk score that
approximates the equation-based
one.)
0.8%
The 10 years General CV Risk Score
Circulation. 2008;117:743-753.
14. Lifetime Risks of Cardiovascular Disease
Jarett D. Berry, M.D., Alan Dyer, Ph.D., Xuan Cai, M.S., Daniel B. Garside, B.S.,
Hongyan Ning, M.D., Avis Thomas, M.S., Philip Greenland, M.D., Linda Van Horn,
R.D., Ph.D., Russell P. Tracy, Ph.D., and Donald M. Lloyd-Jones, M.D.
N Engl J Med 2012; 366:321-329January 26, 2012
Background
The lifetime risks of cardiovascular disease have not been
reported across the age spectrum in black adults and white
adults.
Conclusions
Differences in risk-factor burden translate into marked
differences in the lifetime risk of cardiovascular disease, and
these differences are consistent across race and birth
cohorts. (Funded by the National Heart, Lung, and Blood
Institute.)
15. What do you think about this
patient ?
Lifetime Risk
50 %
16. What do you think about this
patient ?
Lifetime Risk
69 %
17. Future CV Risk Prediction:
Concept of Lifetime Risk
Lloyd-Jones et al. Circulation 2006; 113: 791-798
Framingham Heart Study: Optimization of RFs in asymptomatic
50 year-olds associated with low lifetime CVD risk
Optimal
Total chol <180
BP <120/80
Nonsmoker
Non diabetic
Not optimal
Total chol 180-200
BP 120-140/80-90
Elevated RF
Total chol 200-240
SBP 140-160/90-100
Major RF
Total chol >240
BP >160/90
Smoker
Diabetic
18. Other issues:
Low
H D L
Diabetes
Metabolic
Syndrome
Inflammation
HsCRP
Triglycerides
Stress
19. Niacin in Patients with Low HDL
Cholesterol Levels Receiving Intensive
Statin Therapy
The AIM-HIGH Investigators
N Engl J Med 2011; 365:2255-2267
In patients with established cardiovascular disease,
residual cardiovascular risk persists despite the
achievement of target low-density lipoprotein (LDL)
cholesterol levels with statin therapy. It is unclear
whether extended-release niacin added to simvastatin
to raise low levels of high-density lipoprotein (HDL)
cholesterol is superior to simvastatin alone in reducing
such residual risk.
20. AIM-HIGH :AIM-HIGH : The trial was stopped after a mean
follow-up period of 3 years owing to a lack of
efficacy.
• Among patients with atherosclerotic cardiovascular
disease and LDL cholesterol levels of less than 70 mg
per deciliter (1.81 mmol per liter), there was no
incremental clinical benefit from the addition of niacin to
statin therapy during a 36-month follow-up period,
despite significant improvements in HDL cholesterol and
triglyceride levels.
• (Funded by the National Heart, Lung, and Blood Institute and Abbott
Laboratories)
21. The “Super-Sizing” of America
“This year, Americans will spend more money on
fast food than on higher education…”
Eric Schlosser.Eric Schlosser. Fast Food Nation: The Dark Side of the All-American MealFast Food Nation: The Dark Side of the All-American Meal..
Harper Collins. 2002.Harper Collins. 2002.
22. Haffner SM, Lehto S, Ronnemaa T, et al: N Engl J Med 339:229–234, 1998
Diabetes is a “cardiovascular disease
risk equivalent”
23.
24. ► Optimal fasting triglyceride levels, defined
as 100 mg/dL, as a parameter of metabolic
health, and
► Non-fasting triglyceride levels can be used
to screen for those with high fasting
triglyceride levels. Normal non-fasting < 200
mg/dL
AHA Scientific Statement on Triglycerides and CVD
This statement suggests the following new designations:
Miller M et al. Circulation. 2011;123 published online Apr 18, 2011; DOI: 10.1161
29. Sir Winston Churchill, 91Sir Winston Churchill, 91 Jim Fixx, 53Jim Fixx, 53 ♥♥
Who Has More Cardiovascular RiskWho Has More Cardiovascular Risk
Factors?Factors?
30. Existing Guidelines (Status Quo):
• Screen for Risk Factors of Atherosclerosis
• Treat Risk Factors of Atherosclerosis
Goal of “ new” Guidelines:
• Screen for Atherosclerosis (the Disease)
regardless of, Risk Factors
• Treat based on the Severity of the Disease
and its Risk Factors
ATHEROESCLEROSIS:
Risk Factor screen Vs the
disease screen
31. Slide 31
Atherosclerosis begins early :Usefulness and
Prognostic Implications of Surrogate Markers
in Atherosclerosis
Risk
factors
Surrogate
markers
Arterial
vascular
symptoms
Clinical
events
(MI,
sudden
death)
Autopsy
LateEarly
Adapted from Crouse JR III. J Lipid Res. 2006;47:1677–1699; Nissen S. Am J Cardiol. 2001;87(suppl):15A–20A.
32. Importance of
Subclinical Disease Detection
• Atherosclerosis begins early
• can be detected prior to a cardiac event
• Most MI’s -previously <40% stenosis
• plaque rupture and thrombus (blood clot)!
• Stress tests only detects flow-limiting stenoses
(blockages)
• Subclinical disease measures
• target patients for “aggressive primary prevention”
37. From: Coronary Artery Calcium Scanning Should be Used for
Primary Prevention: Title and subTitle BreakPros J Am Coll
Cardiol Img. 2012;5(1):111-118. doi:10.1016/j.jcmg.2011.11.007
38. Coronary Artery CalciumCoronary Artery Calcium
No CalcificationNo Calcification Severe CalcificationSevere Calcification
Left Main
LAD
LCX
AortaAorta
LALA
PAPA
Left Main
LAD
Measurement of CAC may be reasonable for cardiovascular risk
assessment persons at low to intermediate risk (6% to 10% 10-year
risk).
39. Direct in vivo measurement of thickness
of carotid artery wall by B-mode
ultrasound – “arterial biopsy”
Vessel wall thickness correlates with
status of atherosclerosis and
cardiovascular events
Atherosclerosis is a systemic disorder
Disease in carotid artery is predictive of
disease in other vascular beds
Measurement of CA IMT
Adapted from Crouse JR III. J Lipid Res. 2006;47:1677–1699; Espeland MA, et al. Curr Controll Trials Cardiovasc Med. 2005;6:3; Kastelein JJP,
et al. Am Heart J. 2005;149:234–239. .
41. Slide 41
Rotterdam Study
CA IMT Strongly Predictive of MI
*Adjusted for age and gender
Adapted from van der Meer I, et al. Circulation. 2004;109:1089–1094.
1
1.68
2.05
2.91
0
1
2
3
<0.88 0.88–<0.99 0.99–<1.12 ≥1.12
CA IMT, mm
HazardRatio*
(n=1277) (n=1279) (n=1287) (n=1273)
42. ACCF/ACR/AIUM/ASE/ASN/ICAVL/SCAI/SCC
T/SIR/SVM/SVS
2012 Appropriate Use Criteria for Peripheral
Vascular Ultrasound and Physiological
Testing
Part I: Arterial Ultrasound and Physiological Testing:.. it is
uncertain if Carotid Ultrasound should be used in patient with
intermediate Frammingham Risk Score…
J. Am. Coll. Cardiol. published online Jun 11, 2012;
45. Systematic COronary Risk Evaluation (SCORE): based on gender,
age, total cholesterol, systolic blood pressure and smoking status.
Roques F, Michel P, Goldstone AR, Nashef SA. The logistic EuroSCORE.
Eur Heart J. 2003 May;24(9):882-3
46. Can the combination Therapy (SPAA) for Cholesterol and
Blood Pressure Reduce the 10-year Calculated Risk of
Coronary Heart Disease, Fatal Cardiovascular Disease ?
Zamorano and Edwards, Integrated Blood pressure Control 2011,4:55-71
Editor's Notes
Early statin trials evaluated patients with hypercholesterolemia in both the primary and secondary prevention settings. Subsequent trials extended this to patients with a broad range of cholesterol levels. The MIRACL trial was the first to evaluate the immediate effect of statins in the setting of an acute coronary syndrome. More recent trials have evaluated intensive LDL-C reduction in patients with acute coronary syndromes and chronic coronary heart disease.
Don Lloyd-Jones and colleagues at the Framingham Study have performed a very useful analysis that will likely be incorporated into future CV risk prediction guidelines. They used risk factors assessed at age 50 years for asymptomatic subjects in the FHS and lifetime CVD risk was predicted up to age 95. This slides shows that lifetime risk in women with optimized risk factors is low (8%). Whereas those with at least one not optimal RF have a 27% lifetime risk of CVD and those with elevated or major coronary RFs have a 39-50% lifetime risk of CVD.
We are all aware of the bombardment of over- and super-sized portions, not to mention the explosion of fast-food establishments.
Eric Schlosser. Fast Food Nation: The Dark Side of the All-American Meal. Harper Collins. 2002.
Haffner SM, Lehto S, Ronnemaa T, et al: Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infraction. N Engl J Med 339:229–234, 1998 Probability of death from CHD in diabetic and nondiabetic people with and without prior MI
Content Points:
As discussed earlier, hypertension is often found in conjunction with diabetes.
People with diabetes need to receive appropriate treatment to reduce risk of CVD because they have a marked increase in risk. A person with diabetes has a 2- to 4-fold greater risk of developing CHD than a nondiabetic individual.118
This high risk translates into increased mortality. As shown in the graph, chance of survival for a person with diabetes who has not had an MI is similar to that of a person without diabetes who has already experienced an MI.
Adjustment for LDL-C, HDL-C, triglyceride, smoking and hypertension do not change these results significantly.
Chances of survival drop substantially once an individual with diabetes experiences an MI.
Atherosclerotic disease may be clinically silent for many years before manifesting as a catastrophic clinical event, such as myocardial infarction or sudden death, as it does in over 50% of cases.1,2 Atherosclerotic disease that manifests as arterial vascular symptoms has already progressed well along the disease continuum.
Since early identification and quantification of risk can improve patient management before the onset of clinical manifestations, the use of surrogate markers of atherosclerosis has grown substantially in the past 20 years.1,3 Researchers have developed several ways to measure atherosclerosis progression in an untreated state and its regression with effective treatment. These measures include wall thickness, such as CA IMT; extent of stenosis; presence and dimension of plaque; composition of plaque; and plaque dynamics.1
Surrogate markers based on these measures can provide predictive information regarding clinical endpoints of morbidity and mortality. They can also quantify the beneficial effects of therapy in relatively short periods of time compared with the emergence of clinical endpoints, which may take many years.1,4
A recent study evaluated the prognostic value of hsCRP throughout the range of hsCRP values. Baseline CRP levels were measured in 27,939 healthy women enrolled in the Women’s Health Study. These women were followed over a 9-year period for the occurrence of first cardiovascular events. This figure demonstrates that hsCRP provides useful prognostic information across the range of hsCRP values.
The Rotterdam study determined that CA IMT was a strong, independent predictor of myocardial infarction.1 This slide displays the association between severity of atherosclerosis, defined on the basis of CA IMT, and the hazard ratio for incident myocardial infarction through 7 to 10 years of observation.1
Subjects in the lowest CA IMT quartile (&lt;0.88 mm) were judged to have no atherosclerosis and assigned a hazard ratio for myocardial infarction of 1. Increasing CA IMT values in the other quartiles were clearly associated with increased risk of myocardial infarction. Compared with subjects who had no atherosclerosis, those with mild atherosclerosis (CA IMT 0.88 – &lt;0.99 mm) had a hazard ratio of 1.68. Moderate atherosclerosis (CA IMT 0.99 – &lt;1.12 mm) more than doubled the risk of myocardial infarction, as shown by the hazard ratio of 2.05 relative to the quartile with no atherosclerosis. Severe atherosclerosis (CA IMT ≥1.12 mm), was associated with a hazard ratio for myocardial infarction of 2.91 compared with the lowest quartile, indicating that severe atherosclerosis nearly triples the risk of myocardial infarction.
Study Design
The Rotterdam study was a prospective, population-based study designed to explore the incidence and determinants of chronic diseases. The study cohort comprised 7983 men and women 55 years of age and older at study entry who lived in a suburb of Rotterdam, the Netherlands. Evaluation of CA IMT was made at a baseline examination for each subject between 1990 and 1993, with follow-up evaluations and health data, including incident myocardial infarction, collected through January 1, 2000.1