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Hypertension management- Angina IHD

Hypertension management- Angina IHD

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HYPERTENSION
MANAGEMENT-ANGINA
IHD
Dr. DEV PAHLAJANIDEV PAHLAJANI
MD,FACC,FSCAI
HOD INTERVENTIONAL CARDIOLOGY BREACH
CANDY HOSPITAL MUMBAI
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
“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
ANGINA MANIFESTATIONS
PRINCIPLES OF MANAGEMENT
• Reduce myocardial oxygen consumption
• Reduce bp & after load
• Reduce pulse rate
• Reduce platelet aggregation.
• Reduce contractility
• Vasodilation
• Improve lv function
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
Ad

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Hypertension management- Angina IHD

  • 1. HYPERTENSION MANAGEMENT-ANGINA IHD Dr. DEV PAHLAJANIDEV PAHLAJANI MD,FACC,FSCAI HOD INTERVENTIONAL CARDIOLOGY BREACH CANDY HOSPITAL MUMBAI
  • 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
  • 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%)
  • 15. Antihypertensive Efficacy Mean Blood Pressure Nifedipine GITS Diuretic Combination 138 mmHg 82 mmHg 180 160 140 120 100 80 60 0 2 4 8 12 18 36 70 87 121 138 173 190 225 242 mmHg Year 1 Year 2 Year 3 Year 4 Week Systolic Diastolic 176 mmHg 99 mmHg
  • 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
  • 22. MERIT HF – ALL-CAUSE MORTALITY
  • 23. Carvedilol Or Metoprolol European Trial COMET 17% Lancet 2003; 362: 7-13
  • 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%
  • 28. Copernicus : major outcomes Carvedilol (n = 1156) placebo (n=1133) RR All-cause mortality 11 % 17 % 35 % Hosp. + Mortality 37 % 45 % 24 %
  • 29. CARVEDILOL – EFFECT ON MAJOR CLINICAL EVENTS
  • 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
  • 33. BETA BLOCKERS IN ANGINA • Reduce myocardial oxygen consumption • Reduce heart rate • Reduce BP • Reduce double product • Reduce CAT. • Antiplatelet Effect
  • 34. CALCIUM BLOCKERS • Decrease BP • Vasodilatation • Nefedipine felodipine and amlodipine cause tachycardia
  • 35. Mortality benefits for ACEI trials AMI AMI with LVD CHF TRIAL ACEI Dose† ISIS IV capto 50x2 GISSI 3 lisino 10 SAVE capto 50x2 AIRE rami 5x2 TRACE trandola 4 CONSENSUS enala 40 SOLVD enala 20 .84 .74-.95 .73 .56-.95 .78 .67-.91 .73 .60-.89 .81 .68-.97 .88* .79-.99 .93* .87-.99 RR5%CI *odds ratio †maximum daily
  • 36. 0 0.1 0.2 0.3 0.4 0 1 2 3 4 5 number at risk ACE inhibitors 2995 2250 1617 892 223 Placebo 2971 2184 1521 853 138 time since randomization (years) cumulativemortality(%) placebo Meta-analysis of AIRE, TRACE, SAVE Flather MD, et al. Lancet 2000; 355(9215):1575 - 81 26% reduction p < 0.0001 ACE Inhibitors
  • 37. CV Disease Risk Doubles with Each 20/10 mm Hg BP Increment* *Individuals aged 40-70 years, starting at BP 115/75 mm Hg. CV, cardiovascular; SBP, systolic blood pressure; DBP, diastolic blood pressure CV disease risk SBP/DBP (mm Hg) 0 1 2 3 4 5 6 7 8 115/75 135/85 155/95 175/105 Lewington S, Cardiovascular Issues in Ageing Pilots. et al. Lancet. 2002; 60:1903-1913
  • 38. 38 Diseases Attributable to Hypertension Adapted from: Arch Intern Med 1996; 156:1926-1935. All Vascular
  • 39. JNC VII Classification CategoryCategory SBP (mm Hg)SBP (mm Hg) DBP (mm Hg)DBP (mm Hg) Normal < 120 < 80 Pre – hypertension 120-139 80-90 Hypertension Stage 1 140 – 159 90 – 99 Stage 2 160 and above 100 and above
  • 40. AA, aldosterone antagonist; ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin II-receptor blocker;AA, aldosterone antagonist; ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin II-receptor blocker; ββB,B, ßß-- blocker; CCB, calcium channel blocker; MI, myocardial infarction;blocker; CCB, calcium channel blocker; MI, myocardial infarction; CAD, coronary artery disease. Chobanian AV, et al.CAD, coronary artery disease. Chobanian AV, et al. JAMA.JAMA. 2003;289(19):2560-2572.2003;289(19):2560-2572. The Seventh Report of the Joint National Committee CompellingCompelling IndicationsIndications DiureticDiuretic ßBßB ACEIACEI ARB CCBCCB AAAA Heart failureHeart failure      Post-MIPost-MI    High CAD riskHigh CAD risk     DiabetesDiabetes      Chronic kidneyChronic kidney diseasedisease   Recurrent strokeRecurrent stroke preventionprevention  
  • 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)
  • 45. COMET
  • 46. DRUGS : CARVEDILOL 3.125 MG BID TARGET DOSE 25 MG BID METOPROLOL 5 MG BIDTARGET DOSE 50 MG BID ACE-I & DIURETICS USED CONCURRENTLY COMET TRIAL
  • 47. Carvedilol Or Metoprolol European Trial COMET Lancet 2003; 362: 7-13
  • 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
  • 52. EFFECT OF ß-BLOCKADE BY AETIOLOGY AND NYHA CLASS
  • 53. PHARMACOLOGIC DIFFERENCES ß1 Blockade ß2 Blockade α1 Blockade ISA Ancillary effects * Carvedilol +++ +++ +++ - +++ Metoprolol +++ - - - - Bisoprolol +++ - - - - Bucindolol +++ +++ - + - * Anti- oxidant, anti-endothelin, anti-proliferative
  • 54. CARVEDILOL – EFFECT ON MAJOR CLINICAL EVENTS
  • 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
  • 59. 4 3 2 1 0 -1 -2 -3 -4 4 3 2 1 0 -1 -2 -3 -4 4 3 2 1 0 -1 -2 -3 -4 4 3 2 1 0 -1 -2 -3 -4 mm Hg mm Hg Sildenafil (n=965) Placebo (n=503) Sildenafil (n=386) Placebo (n=244) Change in SBP Change in DBP Change in SBP Change in DBP Blood pressure changes in patients not on antihypertensive therapy (top) and in those receiving 1 of 5 classes of antihypertensive drugs (bottom) during concurrent treatment With sildenafil or placebo. DBP = diastolic blood pressure; SBP = systolic blood pressure. Data on file, Pfizer Inc. B) Antihypertensive drugs A) No Antihypertensive
  • 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

Editor's Notes

  1. 11
  2. 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.
  3. 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 &lt; .0001). The patients with plasma norepinephrine &gt; 900 pg/mL had a higher mortality than those with corresponding values &lt; 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
  4. 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.
  5. 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.
  6. 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 (&lt;140/90 mm Hg, or &lt;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 &gt;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.
  7. 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 &lt;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 &lt;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 &lt;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.
  8. 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).
  9. 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.  
  10. Drugs