2. May not the elevation of systemic BP be a
natural response to guarantee a more
normal circulation to heart, brain and
kidneys (essential HTN)
-Scott RW 1946
Quoted in Prog. In Cardio.Diseases;2006;48(5);303-315
3. “Greatest DanGer to a
Man With hiGh BP Lies in
its Discovery, Because
then soMe FooL is certain
to try anD reDuce it”
- Hay, Quoted in
Prog. In Cardio. Disease; 2006; 48(5);303-315
5. PRINCIPLES OF MANAGEMENT
• Reduce myocardial oxygen consumption
• Reduce bp & after load
• Reduce pulse rate
• Reduce platelet aggregation.
• Reduce contractility
• Vasodilation
• Improve lv function
6. HTN+ANGINA MANAGEMENT GOALS
• Relief of symptoms
• CONTROL HTN TARGET LEVELS TO
Reduce LV mass
Reduce death
Improve endothelial function, reduce
death, MI,HF,REVASC,CVD,CKD
7. Hemodynamic and Electrophysiologic
Changes of CCBs done
Hemodynamic and Electrophysiologic effects of Calcium antagonists
Nifedipine (a) Diltiazem Verapamil
Coronary dilation ++ ++ +
Peripheral dilation ++++ ++ +++
Negative inotropic + ++ +++
AV conduction +++ ++++
Heart rate
Blood pressure ++++ ++ +++
Sinus node
depression
++ ++
Cardiac output ++
a- or other dihydropyridines
+, minimal effect; ++++, maximal effect; , no significant
change; ,decrease; , increase
8. Calcium channel blockers
• Dihydropyridine CCBs are widely used to treat hypertension and ischemic
heart disease
• They inhibit L-type calcium channels found in vascular smooth muscle,
dilating the arterioles
• Meta-analysis of several trials involving newer CCBs (amlodipine,
felodipine, isradipine, nicardipine, or nisoldipine) found higher risk of
mortality compared to other antihypertensive drugs
• Nifedipine
– Extensively evaluated drug
– Favorable effects on CV mortality or morbidity with long-lasting
formulations
9.
10. Reversal of Endothelial Dysfunction
A Promising New Approach to Reduce Vascular Complications
STATINS
CALCIUM ANTAGONISTS
ACE-INHIBITORS
BETA BLOCKER
(Maximum clinical evidence
with Long-acting Nifedipine)
(Clinical evidence
with Nebivolol)
Reversal of
Endothelial Dysfunction
ATHEROPROTECTION
REVERSAL OF VASCULAR REMODELING
ARB
11. Nifedipine XL - Reversal of Endothelial Dysfunction
ENCORE - I Trial
(Effect of Nifedipine and Cerivastatin on recovery of Coronary Endothelial
function)
Study Design:
• Randomized, Placebo-controlled, Double Blind Multi-centric Clinical Trial Carried Out
Across Europe, Israel and Australia
• 800 Coronary Artery Disease Patients (Selected for Angioplasty) Randomized to 4 Groups
(n=200/Group)
* Placebo * Nifedipine XL (30-60mg/d)
* Cerivastatin * Nifedipine XL + Cerivastatin
• Coronary Endothelial Function Assessed at The Beginning and
at the End of 6 Months Treatment Using Acetylcholine Testing
• Blood Flow Velocity and Coronary Diameter Was Measured Using Flowmapping and
Quantitative Angiography Techniques
The ENCORE Investigators .Circulation. 2003;107:422
12. Nifedipine XL - Reversal of Endothelial Dysfunction
ENCORE - I Trial
(Effect of Nifedipine and Cerivastatin on recovery of Coronary Endothelial
function)
Study Results:
*Treatment With Nifedipine XL (Alone) Was Associated With Significant 90%
Improvement in Coronary Endothelial Function as Compared to Placebo
The ENCORE Investigators .Circulation. 2003;107:422
13. Nifedipine and athero-protection coronary calcification
study
Hypertension, 2001, 37(6), 1410-1413
Aim:
To detect the changes in calcium deposition score in coronary arteries of patients
using sophisticated double-helix CT scanning
(Calcium deposition score is an index of atherosclerosis and is directly proportional
to the burden of atherosclerosis)
Findings:
nifedipine XL was associated with significantly slower progression of coronary
calcification in 3 years as compared with diuretic treatment, despite equivalent B.P.
reduction in both arms
14. Nifedipine and athero-protection
American J. Cardiology, 1989.
113 patients ISDN with recent onset, stable angina, followed up
for 2 years, Nifedipine v/s Propranolol v/s Progression, Steadiness
and Regression of Coronary Disease
* The number of stenoses with evidence of progression was significantly smaller after nifedipine.
Nifedipine
N=39
Propranolol
N= 36
ISDN
N=38
No. of
patients with
progression
12 (31%) * 19(53%) 18(47%)
No. of
patients with
steadiness
20(51%) 14 (39%) 17 (45%)
No. of
patients with
regression
7(18%) 3(8%) 3(8%)
16. Angina Pectoris, Transient Ischemic Attacks
(TIAs), Renal Failure
Individual Secondary Endpoints (Non-fatal)
0
0.5
1.0
1.5
2.0
2.5
%ofPatients
0.3 0.4
Angina pectoris TIAs Renal Failure*
p = 1.0 p = 0.38
Nifedipine GITS
Diuretic Combination
3.0
1.8
0.8 0.8
2.4
*Decrease in estimated GFR > 25% compared to value at inclusion at 2 repeated measures
0
0.5
p = 0.10
17. CASE BASED HYPERTENSION
MANAGEMENT (CASE 1)
• 65 yrs.Male
• H/o anterior wall MI 6yrs.Back
• Had post MI angina
• CABGS 5yrs. back
• SOB Class 2
• BP 176/76,LVEF 35%
• NON DM,CREAT.1.4
18. Effect of ACE-I in post MI patients
with HF or LV dysfunction
Mortality
• SAVE: 25% (placebo) vs 20% (captopril) - 19% RRR
• AIRE: 23% (placebo) vs 17% (ramipril) - 27% RRR
• TRACE: 42.3% (placebo) vs 34.7% (trandolapril)- 24% RRR
19. Study Patient population Randomized to Results
ACE-I-Intolerant
CHARM-Alternative NYHA II-IV
ACE-I intolerant patients
Candesartan vs. placebo 23% RRR in primary endpoint (CV
death + CHF hospitalize)
On ACE-I,PLUS ARB
CHARM-Added NYHA II-IV Candesartan vs. placebo 15% RRR in primary endpoint (CV
death + CHF hospitalize)
Val-Heft NYHA II-IV Valsartan vs. placebo No mortality difference (but 13%
RRR in mortality + morbid)
ACE-I vs. ARB
ELITE I NYHA II-IV Losartan vs. captopril 46% risk reduction in all cause
mortality with losartan (secondary
outcome)
ELITE II NYHA II-IV Losartan vs. captopril No mortality difference
No difference in CHF admissions
OPTIMAAL Post MI LV dysfunction Losartan vs. captopril Trend towards better outcomes
all cause mortality (p= 0.7), SCD
(p=0.7), in captopril group
VALIANT Post MI LV dysfunction Valsartan vs. captopril No difference in all cause
mortality or CV morbidity and
mortality
ARB Trials
20. Eichhorn EJ, JCF. 2000;6(suppl 1):40-46.
LVEF
Time (months)
Biologic
Effect
Pharmacologic Effect
b-Blocker
Initiated
b-Blocker Discontinued
00 11 33 66 88
β-Blocker Effects
On Ejection Fraction in Heart Failure
21. Mortality by Baseline Plasma
Norepinephrine Level (PNE)
Francis G et al. Circulation. 1993;87(suppl VI):VI-40 - VI-48.
100
80
60
40
20
0 6 12 18 24 30 36 42 48 54 60
Months
CumulativeMortality(%)
PNE > 900 pg/mL
PNE > 600 and < 900 pg/mL
PNE < 600 pg/mL
2 Year
P < .0001
Overall
P < .0001
0
24. Per cent of patients able to tolerate carvedilol treatment,
grouped according to traditional contraindications and
precautions in prescribing a β-blocker
88 85 86 84
12 15 14 16
0
20
40
60
80
100
Allpatients
(n=795)
COPD/asthma
(n=89)
Diabetes
(n=127)
PVD(n=58)
Tolerated Not Tolerated
Percent
Heart 2000; 84:615-619
25. EPHESUS
• 6642 patients:
a) 3-14 days post MI,
b) EF<40,
c) CHF (rales, pulmonary venous congestion seen
on CXR, 3rd heart sound) OR Diabetes
• randomized to 25 mg eplerenone titrated up
to 50 mg po qd
NEJM 2003;348:1309-21
26. EPHESUS
• Results:
– One year mortality: 15% risk reduction (11.8% vs 13.6%)
– CV death or cardiovascular hospitalizations (26% vs 30.0%)
• (75% of patients on beta blockers)
• adverse effects:
– serious hyperkalemia (K>6) Epler- 5.5% vs plac- 3.9% (p=.002)
– serious hypokalemia (K<3.5) Epler- 8.4% plac- 13.1% (p<.001)
– gynecomastia- 0.5% vs 0.6%
30. • Results:
• 46% mortality placebo vs
35% spironolactone (30%
RRR)
• adverse effects:
– 10% of pts in
spironolactone group
developed
gynecomastia.
– -serious hyperkalemia
(K>6) 14% vs 10% (not
statist sig)
RALES
31. Spironolactone-induced reduction in systolic (dark blue
cones) and diastolic blood pressure (red cones) at 6 weeks,
3months, and 6months of follow-up in subjects with
resistant hypertension done
32. CASE 2
• Male 54 yrs obese built increased ABD girth
• Angina on effort class ii
• HTN BP 206/92,pulse 92/min
• Coronary ANGIO OM CX 70%.PD 70% EF 55%
• Advanced medical treatment and SOS PTCA with
stents
41. JNC 7: Algorithm for Treatment of
Hypertension
Prehypertension (SBP 120-139 mm Hg or DBP 80-89 mm Hg)
Not at Goal BP (<140/90 mm Hg, or <130/80 mm Hg for
patients with diabetes or chronic kidney disease)
Without Compelling Indications With Compelling Indications
Prehypertension
Stage 1 Hypertension
(SBP 140-159 or DBP 90-99 mm Hg)
Thiazide-type diuretics for most;
may consider ACEI, ARB, BB,
CCB, or combination.
Stage 2 Hypertension
(SBP ≥160 or DBP ≥100 mm Hg)
2-drug combinations for most
(usually thiazide-type diuretics and
ACEI, or ARB, or BB, or CCB).
Drug(s) for compelling indications
Other antihypertensive drugs
(diuretic, ACEI, ARB, BB, CCB)
as needed.
LIFESTYLE MODIFICATIONS
If not at goal BP, optimize dosages or add additional drugs until
goal BP is achieved. Consider consultation with hypertension specialist.
INITIAL DRUG CHOICES
42. HF of Ischemic EtiologyHF of Ischemic EtiologyHF of Ischemic EtiologyHF of Ischemic Etiology
ACS - STEMIACS - STEMIACS - STEMIACS - STEMI
ACS – UA and NSTEMIACS – UA and NSTEMIACS – UA and NSTEMIACS – UA and NSTEMI
CAD and Stable AnginaCAD and Stable AnginaCAD and Stable AnginaCAD and Stable Angina
Primary PreventionPrimary PreventionPrimary PreventionPrimary Prevention
Diagnosis
Rosendorff et al.Rosendorff et al. Circulation.Circulation. 2007;115:2761-2788.2007;115:2761-2788.
ASC: acute coronary syndrome, UA: Unstable angina, NSTEMI: Non-ST segment elevation myocardial infarction, STEMI: ST
segment elevation myocardial infarction, HF: Heart failure
<130/80, but consider <120/70<130/80, but consider <120/70<130/80, but consider <120/70<130/80, but consider <120/70
<130/80<130/80<130/80<130/80
<130/80<130/80
Diabetes, Chronic Kidney Disease, CAD, CADDiabetes, Chronic Kidney Disease, CAD, CAD
Equivalents, or Framingham Risk ScoreEquivalents, or Framingham Risk Score ≥10%≥10%
<130/80<130/80
Diabetes, Chronic Kidney Disease, CAD, CADDiabetes, Chronic Kidney Disease, CAD, CAD
Equivalents, or Framingham Risk ScoreEquivalents, or Framingham Risk Score ≥10%≥10%
Target BP (mm Hg)
<140/90<140/90<140/90<140/90
AHA Scientific Statement—Treatment of
Hypertension in the Prevention and Management of
Ischemic Heart Disease
43. Phase ofPhase of
TreatmentTreatment
AcuteAcute
treatmenttreatment
SecondarySecondary
preventionprevention
OverallOverall
Total #Total #
PatientsPatients
28,97028,970
24,29824,298
53,26853,268
0.50.5 1.01.0 2.02.0
RR of deathRR of death
b-blocker betterb-blocker better
RR (95% CI)RR (95% CI)
Placebo betterPlacebo better
0.87 (0.77-0.98)0.87 (0.77-0.98)
0.77 (0.70-0.84)0.77 (0.70-0.84)
0.81 (0.75-0.87)0.81 (0.75-0.87)
β−blocker Evidence: Secondary Prevention
Antman E, Braunwald E. Acute Myocardial Infarction. In: Braunwald E, Zipes DP,Antman E, Braunwald E. Acute Myocardial Infarction. In: Braunwald E, Zipes DP,
Libby P, eds. Heart Disease: A textbook of Cardiovascular Medicine, 6th ed.,Libby P, eds. Heart Disease: A textbook of Cardiovascular Medicine, 6th ed.,
Philadelphia, PA: W.B. Sanders, 2001, 1168.Philadelphia, PA: W.B. Sanders, 2001, 1168.
Summary of Secondary Prevention Trials of b-blocker TherapySummary of Secondary Prevention Trials of b-blocker Therapy
CI=Confidence interval, RR=Relative riskCI=Confidence interval, RR=Relative risk
44. ––22%22% ––20%20% ––20%20%
Hanes DS et al.Hanes DS et al. J Clin Hypertens (Greenwich).J Clin Hypertens (Greenwich). 2001;3(4):236-243.2001;3(4):236-243.
Risk Reduction With β-Blockers
in Post-MI Patients
––30%30%
––40%40%
––20%20%
––10%10%
0%0%
––33%33%
OverallOverall
mortalitymortality
SuddenSudden
cardiaccardiac
deathdeath
Non-suddenNon-sudden
deathdeath Nonfatal MINonfatal MI
15 Trials (n =18,995)15 Trials (n =18,995)
48. • 2647 patient
• Ischaemic or non ischaemic
• Moderate to severe HF (class III NYHA)
• Bisoprolol upto 10 mg day or placebo
• Conventional therapy
• Upto 28 months (average 16 months)
Cardiac insufficiency bisoprolol study
CIBIS-II
Lancet 1999 353; 913
49. SURVIVAL CURVE – CIBIS II
~ 30 % reduction of
all-cause mortality
50. BEST
ß-BLOCKER EVALUATION SURVIVAL TRIAL
• N = 2708 patients
• Survival in patients with moderate to severe heart
failure
– NYHA III – IV
– EF < 35 %
51. BEST : MAJOR OUTCOMES
Bucindolol
(n=1263)
Placebo (n=1260) Risk reduction
All cause mortality 30.2 %
(Annualised
rate 14.9%)
33.0% (Annualised
rate 16.6.%)
8.5% (NS)
Cardiovascular
mortality*
24.4% 27.9% 12.5% (p= 0.04)
All hospitalisation 61% 64% 4.7% (NS)
Heart failure
hospitalisation
35% 42% 16.7% (p=0.001)
Progression to death/
transplant
31.6% 35% 10% (NS)
* No significant difference in death due to heart failure, sudden
death, pump failure or myocardial infarction
56. EVENT-FREE SURVIVAL IN THE TWO GROUPS WITH (THICK LINE)
AND WITHOUT (THIN LINE) ECHOCARDIOGRAPHIC LVH AT THE
BASELINE
BSA INDICATES BODY SURFACE AREA
ProbabilityofEventFreeSurvival
100
90
80
70
60
4
3
2
1
0
RateofEvents(per100patient-years
Baseline LV mass > 125 g/BSA
Baseline LV mass < 125 g/BSA
p = 0.013
0 100 200 300 400 500 < 125 > 125
Time to Event, week Baseline LV mass, g/BSA
57. EVENT RATE IN SUBSET WITH ECHOCARDIOGRPHIC
LVH ATE BASELINE VISIT
0 100 200 300 400 500 Regressors Non Regressors
Time to Event, week
ProbabilityofEventFreeSurvival%
7
6
5
4
3
2
1
0
RateofEvents(per100patient-years
100
90
80
70
60
50
40
Regressors (N=52)
Non regressors (N=60)
p = 0.002
Circ. 1998, 97, 48
Baseline LV mass > 125 g/BSA
Follow-up mass < 125 g/BSA
Baseline LV mass > 125 g/BSA
Follow-up mass > 125 g/BSA
58. SOME DRUGS THAT MAY CAUSE
ERECTILE DYSFUNCTION
Group Group
Antihypertensive Diuretics
Vasodilators e.g. hydralazine
Central sympatholytics,
e.g. methyldopa, clonidine,
reserpine
Ganglion blockers e.g.
guanethidine
Beta-Blockers
Calcium antagonists
ACE inhibitors
Lipid-modifying agents Clofibrate
Antimicrobials Ethionamide, Vidarabine
Cardiac-active agents Digoxin
Gastrointestinal agents Cimetidine
62. Cilnidipine – Heart Rate
• Study conducted in 2920 hypertensive patients:
– Treatment with cilnidipine and ARBs showed
significant reductions in heart rate
• 24-h ambulatory blood pressure monitoring study
with hypertensive patients
– Reductions in heart rate significantly greater in the
cilnidipine group than the amlodipine group
Nagahama S, et al. Hypertens Res 2007;30:815–822
63. Effects of cilnidipine on
norepinephrine (NE) secretion
Cilnidipine attenuates norepinephrine release from sympathetic
nerve endings
Takahara A. Cardiovascular Therapeutics 2009; 27; 124–139
64. Cilnidipine Summary of Effects
• Inhibits sympathetic N-type Ca2+
channels and vascular L-type
Ca2+
channels
• Does not suppress cardiac functions at vasodilator doses
– Shows antisympathetic profiles
– Comparable BP reduction
• Better reduction of heart rate
• More vascular effect than cardio effect
• Favorable effect on glucose homeostasis
• Improves glomerular filtration, renal protection
• Reduces proteinuria
11 Slide 11 This slide is a schematic representation of the time course effects of - blocker therapy on the ejection fraction in patients with heart failure. The pharmacologic effect of - blockade is characterized by relatively small, acute fluctuations in ejection fraction. During initiation of -blockade therapy, these small fluctuations may contribute to acute exacerbation of heart failure symptoms. However, within 1 to 3 months, the biological effects (reverse remodeling) of - blockade begin to appear and ejection fraction increases. The biologic effects of - blockade are reversed if - blockade is discontinued. 1 To date, the vast majority of clinical trials that have reported LVEF measurements have shown significant improvement in LVEF with - blocker therapy. This increase in LVEF is consistent across studies, regardless of underlying cardiac cause (i.e., ischemic, idiopathic cardiomyopathy, or mixed cause) or the - blocker studied (e.g., TOPROL-XL, carvedilol and others). These findings suggest that improvement of LVEF is a - blocker class effect that is independent of heart failure cause. 2 Slide and Notes References 1. Eichhorn EJ. Medical therapy of chronic heart failure. Role of ACE inhibitors and beta-blockers. Cardiol Clin. 1998;16:711-725. 2. Eichorn EJ, Bristow MR. Medical therapy can improve the biological properties of the chronically failing heart. A new era in the treatment of heart failure. Circulation . 1996;94:2285-2294. 3. Eichhorn EJ. Clinical use of -blockers in patients with heart failure. J Cardiac Fail . 2000;6:40-46.
Slide 10 Heart failure patients demonstrate long-term activation of the sympathetic nervous system. The level of adrenergic nervous system activation correlates with the concentration of plasma norepinephrine, as well as with levels of left ventricular filling pressures and mean right atrial pressure. 1 The extent of elevation of plasma norepinephrine concentration occurring in patients with heart failure correlates directly with the severity of left ventricular dysfunction, 2 and with cardiac mortality. 3 Measurements of plasma norepinephrine and plasma renin activity were performed in the Vasodilator-Heart Failure Trial II (V-HeFT II) to assess the effect of therapy on neuroendocrine activation and examine the response to therapy among patients with different degrees of activation. Baseline plasma norepinephrine data were grouped into three relatively homogeneous strata for analysis. Cumulative mortality between the three strata was significantly different ( P < .0001). The patients with plasma norepinephrine > 900 pg/mL had a higher mortality than those with corresponding values < 600 pg/mL or from 601 to 900 pg/mL. In these three groups mortality was directly related to increased plasma norepinephrine levels. This study thus confirms the relationship between baseline PNE values and cumulative mortality in heart failure patients. 4 Slide and Notes References 1. Leimbach WN Jr, Wallin G, Victor RG, et al. Direct evidence from intrarenal recordings for increased central sympathetic outflow in patients with heart failure. Circulation . 1986;73:913-919. 2. Thomas JA, Marks BH. Plasma norepinephrine in congestive heart failure. Am J Cardiol . 1978;41:233-243. 3. Cohn JN, Levine TB, Olivari MT, et al. Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med. 1984;311:819-823. 4. Francis GS, Cohn JN, Johnson G, et al. Plasma norepinephrine, plasma renin activity, and congestive heart failure. Relations to survival and the effects of therapy in V-HeFT II. The V-HeFT VA Cooperative Studies Group. Circulation . 1993;87(suppl VI):VI-40–VI-48. 10
Slide Summary According to a meta-analysis of over 60 prospective studies, the risk of cardiovascular disease doubles with each rise of 20 mm Hg in systolic blood pressure (BP) and 10 mm Hg in diastolic BP. Background In a meta-analysis of 61 prospective, observational studies conducted by Lewington et al involving one million adults with no previous vascular disease at baseline, the researchers found that between the ages of 40-69 years, each incremental rise of 20 mm Hg systolic BP and 10 mm Hg diastolic BP was associated with a twofold increase in death rates from ischemic heart disease and other vascular disease. The researchers also noted that when attempting to predict vascular mortality risk from a single BP measurement, the average of systolic and diastolic BP was “slightly more informative” than either alone, and that pulse pressure was “much less informative.” The seventh report Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) notes this study result as yet more information linking hypertension to high risk for cardiovascular events. Lewington S, Clarke R, Qizilbash H, et al. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet . 2003;361:1903-1913. JNC 7. JAMA. 2003;289:2560-2572.
Slide 5 Studies show that a multitude of diseases are attributable to hypertension. They include: • Heart failure • Coronary heart disease • Myocardial infarction • Left ventricular hypertrophy and failure • Aortic aneurysm • Peripheral vascular disease • Retinopathy • Hypertensive encephalopathy • Chronic kidney failure • Cerebral hemorrhage • Stroke With so many diseases linked to hypertension, prompt and effective treatments have the potential to reduce many complications. Dustan HP, et al. Arch Intern Med 1996; 156:1926-1935.
Partners in Healthcare Education, LLC 2009 Health-promoting lifestyle modification(s) should be applied in persons with prehypertension as primary prevention. These nonpharmacologic treatments, such as diet and exercise, should also be encouraged in patients with all stages of hypertension, as they may enhance the efficacy of antihypertensive agents and minimize risk factors associated with hypertension. While lifestyle modifications are helpful, pharmacologic therapy is usually needed to treat high BP. Most patients with hypertension require 2 antihypertensive agents to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease). A thiazide-type diuretic is recommended as initial therapy for uncomplicated hypertension, either alone or in combination with an antihypertensive agent from another class (ACEI, angiotensin receptor blocker [ARB], β- blocker, or CCB). A drug from a different class should be added if the first drug is insufficient for achieving goal BP. Patients whose BP is >20/10 mm Hg above goal should receive pharmacologic therapy, either singly or in a fixed-dose combination. National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure . Bethesda, Md: National Heart, Lung, and Blood Institute; 2003. NIH Publication No. 03-5233.
MAIN MESSAGE: BP targets for high risk individuals are lower than 140/90. In a scientific statement issued by the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention, the panel recommended the following: “ For the primary prevention of CAD in hypertension, aggressive BP lowering is appropriate, with a target BP of <130/80 mm Hg in individuals with any of the following: diabetes mellitus; chronic renal disease; CAD; CAD risk equivalents; carotid artery disease (carotid bruit, or abnormal carotid ultrasound or angiography); peripheral arterial disease; abdominal aortic aneurysm; and for high-risk patients, defined as those with a 10-year Framingham risk score of greater than or equal to 10%; and a target BP of <140/90 mm Hg in individuals with none of the above (Class IIa; Level of Evidence B).” The 130/90 mm Hg BP target is also recommended for patients with CAD and stable angina, acute coronary syndrome (ACS) with unstable angina and non-ST segment elevation MI, or ST segment MI. Patients with heart failure of ischemic etiology have the same target, but <120/80 mm Hg should be considered. [1] Reference 1. Rosendorff C, Black HR, Cannon CP, et al. Treatment of Hypertension in the Prevention and Management of Ischemic Heart Disease. Circulation 2007;115:2761-2788.
Beta blockers reduce the risk of death in individuals with known cardiovascular disease. In a meta-analysis that included 24,298 patients with stable coronary heart disease, treatment with a beta-blocker resulted in a 23% relative risk reduction in the risk of death (95% confidence interval, 0.70-0.84).
Numerous trials have confirmed the benefits of ß-blocker therapy in the post-MI patient. In a meta-analysis of 15 ß-blocker trials, the following risk reductions were seen: Overall mortality: 22% Sudden cardiac death: 33% Nonsudden death: 20% Nonfatal MI: 20% 1 1. Hanes DS, Weir MR. J Clin Hypertens . 2001;3:236–243.
