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Hf. final
- 1. Heart Failure: the changing paradigm The most common reason for hospitalization in adults >65 years old.
- 2. Heart Failure-Heart Failure- Clinical syndrome … can result fromClinical syndrome … can result from any structural or functional cardiac disorder thatany structural or functional cardiac disorder that impairs ability of ventricle to fill with or eject bloodimpairs ability of ventricle to fill with or eject blood Impact!Impact! 5 million patients- have heart failure 500,000 new cases every year 300,000 deaths/year300,000 deaths/year
- 3. Types of Heart Failure • Systolic heart failure (HFrEF) – Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure – EF =<35% • Diastolic heart failure (HFpEF) – Involves a thickened and stiff heart muscle – As a result, the heart does not fill with blood properly – This results in fluid backup in the lungs and heart failure – EF =>50%
- 4. Risk Factors for Heart Failure • Coronary artery disease • Hypertension (LVH) • Valvular heart disease • Alcoholism • Infection (viral) • Diabetes • Congenital heart defects • Other: – Obesity – Age – Smoking – High or low hematocrit level – Obstructive Sleep Apnea
- 5. Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional Class ACC/AHA HF Stage1 NYHA Functional Class2 A At high risk for heart failure but without structural heart disease or symptoms of heart failure (eg, patients with hypertension or coronary artery disease) B Structural heart disease but without symptoms of heart failure C Structural heart disease with prior or current symptoms of heart failure D Refractory heart failure requiring specialized interventions I Asymptomatic II Symptomatic with moderate exertion IV Symptomatic at rest III Symptomatic with minimal exertion None
- 6. Adapted from Cohn JN. N Engl J Med. 1996;335:490–498. Pathologic remodeling Low ejection fraction Death Symptoms: Dyspnea Fatigue Edema Chronic heart failure •Neurohormonal stimulation •Myocardial toxicity Sudden Death Pump failure Coronary artery disease Hypertension Cardiomyopathy Valvular disease Myocardial injury Pathologic Progression of CV Disease Diabetes
- 7. Compensatory Mechanisms:Compensatory Mechanisms: Renin-Angiotensin-Aldosterone SystemRenin-Angiotensin-Aldosterone System Renin + Angiotensinogen Angiotensin I Angiotensin II Peripheral Vasoconstriction ↑ Afterload ↓ Cardiac Output Heart FailureHeart Failure ↑ Cardiac Workload ↑ Preload ↑ Plasma Volume Salt & Water Retention Edema Aldosterone Secretion ACE Kaliuresis BetaBeta StimulationStimulation • COCO • NaNa++ Fibrosis
- 9. Symptoms
- 10. Stage A At high risk for developing heart failure. Includes people with: Hypertension Diabetes mellitus CAD (including heart attack) History of cardiotoxic drug therapy History of alcohol abuse History of rheumatic fever Family history of CMP Exercise regularly Quit smoking Treat hypertension Treat lipid disorders Discourage alcohol or illicit drug use If previous heart attack/ current diabetes mellitus or HTN, use ACE-I Stage B Those diagnosed with “systolic” heart failure- have never had symptoms of heart failure (usually by finding an ejection fraction of less than 40% on echocardiogram Care measures in Stage A + Should be on ACE-I Add beta -blockers Surgical consultation for coronary artery revascularization and valve repair/replacement (as appropriate Stage C Patients with known heart failure with current or prior symptoms. Symptoms include: SOB, fatigue Reduced exercise intolerance All care measures from Stage A apply, ACE-I and beta-blockers should be used + Diuretics, Digoxin, Dietary sodium restriction Weight monitoring, Fluid restriction Withdrawal drugs that worsen condition Maybe Spironolactone therapy Stage D Presence of advanced symptoms, after assuring optimized medical care All therapies -Stages A, B and C + evaluation for:Cardiac transplantation, VADs, surgical options, research therapies, Continuous intravenous inotropic infusions/ End-of-life care Therapies
- 11. Drug Therapy
- 12. Heart Failure Treatments: Medication Types •ACE inhibitor (angiotensin- converting enzyme) •ARB (angiotensin receptor blockers) •Beta-blocker •Digoxin •Diuretic •Aldosterone blockade Type What it does •Expands blood vessels which lowers blood pressure, neurohormonal blockade •Similar to ACE inhibitor—lowers blood pressure •Reduces the action of stress hormones and slows the heart rate •Slows the heart rate and improves the heart’s pumping function (EF) •Filters sodium and excess fluid from the blood to reduce the heart’s workload •Blocks neurohormal activation and controls volume
- 13. Rational for Medications • Improve Symptoms – Diuretics (water pills) – digoxin • Improve Survival – Betablockers – ACE-inhibitors – Aldosterone blockers – Angiotensin receptor blockers (ARB’s)
- 14. Lifestyle Changes •Eat a low-sodium, low-fat diet •Lose weight •Stay physically active •Reduce or eliminate alcohol and caffeine •Quit Smoking What Why •Sodium is bad for high blood pressure, causes fluid retention •Extra weight can put a strain on the heart •Exercise can help reduce stress and blood pressure •Alcohol and caffeine can weaken an already damaged heart •Smoking can damage blood vessels and make the heart beat faster
- 15. • Ivabradine can be beneficial to reduce HF hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤35%) who are receiving GDEM, including a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest. • IIa, ACC/ AHA focused update 2016
- 16. PERIPHERAL ULTRAFILTRATION • Removes sodium and water in hospitalized HF patients who are refractory to pharmacologic therapy. • (UNLOAD) trial enrolled 200 patients with AHFS and reduced or preserved ejection fraction, Dyspnea and renal function were not improved.. • ESC 2016 Class IIb , (Level of Evidence: C)
- 17. Arginine Vasopressin Antagonist • Tolvaptan – oral , selevtive V2 • Conivaptan- i/v , V1a + V2 • Everest trial
- 18. Although tolvaptan and conivaptan have been approved for the treatment of clinically significant hypervolemic and euvolemic hyponatremia, their value in the management of AHFS, with or without hyponatremia, remains to be determined. Class IIb (Level of evidence B)
- 19. Cinaciguat • Soluble guanylate cyclase(sGC) activator • Preliminary studies shows beneficial hemodynamic profile • At higher doses associated with significant hypotension, but did not affect 30 days post discharge mortality • COMPOSE Trial
- 20. Advantages over Nitrates • Heme independent means no tolerance • More predicatable vasodilatory response
- 21. Chimeric Natriuretic Peptides(CD-NP) • C type natriuretic peptide (CNP) • lacks the natriuretic property of ANP and BNP • Less hypotension – primaraly a venodilator • Dendroaspis (DNP) • Significant natriuretic • Cause hypotension – both artery and venodilator
- 22. Aliskiren • Direct renin inhibitor • Approved for treatment of hypertension • Oral treatment • ACE inhibitors and ARBs are of proven benefit in treatment of CHF
- 23. ASTRONAUT • Addition of alikiren to standard therapy delays time to events including CV deaths of HF rehopitalization within 6 mths in pts hospitalized for AHFS and EF < 40 %
- 24. • ATMOSPHERE TRIAL did not establish role of Aliskiren in heart failure
- 25. Rolofylline • Highly selective Adenosine A 1 receptor antagonist • Increases RBF • Enhances diuresis • But does not activate the tubulo glomerular feedback
- 26. • Pilot study was PROTECT trial which showed positive trends in AHF • But PROTECT II showed only mild benefits on symptoms and no effects on renal protection and other pre specified outcomes and was associated with more CNS adverse effects • Hence current status : doubtful
- 27. Ularitide • Synthetic analouge of urodilatin • Urodilatin is natriuretic and diuretic hormone ( ANP family) • Ularitide has additional vasodilatory properties due to effect on vascular c GMP
- 28. • SIRIUS I and II(Safety and Efficacy of an Intravenous Placebo /controlled Randomized infusion of Ularitide in Prospective double blind Study in patients with Symptomatic Decompansated Chronic Heart Failure) • Improved clinical status, hemodynamics and neurohormonal profile • S/E : significant hypotension
- 29. Endothelin antagonists • Endothelin 1 ,2 , 3 • Receptors : ET A and ET B • Most potent endogenous vasoconstriction via ET A receptos • Levels of Endothelin increase in HF and correlates with patient outcomes • Currently aproved for treatement of PAH with moderated dysability (Functional Class III)
- 30. Tezosentan • Non selective ET A/B antagonist • VERITAS trial • > 1400 pts with AHF were given tezosentan infusion 24 – 72 hrs v/s placebo • Did not improve symptoms or decrease mortality at day 7 post randomization
- 31. Istaroxime • Prototype of a new class of drug • M/A : inhibits membrane bound Na+/K+ ATPase and stimulates SERCA 2a • Hence increase inotropic and lusitropic effects • Improves both systolic and diastolic function, reduce LV dimension in diastole and increase SBP
- 32. HORIZON HF trial • Studied 120 pts with AHF and reduced EF • Addition of istaroxime to standard therapy lowered PCWP and heart rate and increased SBP • Higher dose infusion (1.5 mcg/k/min) increased cardiac index and reduced LVEDV • No changes in neurohormones , renal function and trop I levels during 6 hr infusion
- 33. Relaxin • Pre – RELAX – AHF study • Dose response effect of relaxin v/s placebo on symptom relief, other clinical outcomes and safety in pts with AHF and normal to incresed BP • Associated with improvement in dyspnea and other clinical outcomes • Currently being studied in RELAX-AHF trial- phase II/III
- 34. ANTICOAGULATION IN AC HF • HAS BLED • CHA2DS2-VASc • WARCEF trial
- 36. Overview of Device Therapy 36 Biventricular Pacing Ventricular Dysynchrony • Abnormal ventricular conduction resulting in a mechanical delay and dysynchronous contraction
- 37. BiV Pacing
- 39. Cardiac Resynchronization Therapy Key Points Recommendations • CRT is recommended for symptomatic patients with HF in sinus rhythm with a QRS duration ≥150 msec and LBBB QRS morphology and with LVEF ≤35% despite OMT in order to improve symptoms and reduce morbidity and mortality. • Timing of Referral Important – Patients often not on optimal Medical Rx – Patients referred too late- Not a Bail Out
- 41. Heart Failure and Sudden Cardiac Death – SCD is one of the leading causes of death in the U.S. – approximately 450,000 deaths a year – Patients with heart failure are 6-9 times as likely to develop sudden cardiac death as the general population
- 42. How does a defibrillator for sudden cardiac death work?
- 43. Implantable Cardiac Defribrillators EBM Therapies Relative Risk Reduction Mortality 2 year ACE-I 23% 27% Β-Blockers 35% 12% Aldosterone Antagonists 30% 19% ICD 31% 8.5%
- 44. • ICD is recommended in patients: a) with asymptomatic LV systolic dysfunction (LVEF ≤30%) of ischaemic origin, who are at least 40 days after acute myocardial infarction, b) with asymptomatic non-ischaemic dilated cardiomyopathy (LVEF ≤30%), who receive OMT therapy, in order to prevent sudden death and prolong life.
- 45. Other Therapies? • Transplant • Artificial hearts • New “gadgets” to help doctors manage heart failure
- 47. In Summary…. • Heart failure is common and has high mortality • Drug therapy improves survival – Betablockers, ACE-I, aldosterone antagonists • Newer device therapies are showing promise for symptom relief and improved survival – Biventricular pacing, ICD’s • Transplants remain rare, but technology for mechanical assist devices continues to improve, stay tuned …! ! !
- 49. THANKS….
Hinweis der Redaktion
- The major risk factors that are associated with HF are CAD, a history of previous MI, hypertension, valvular heart disease, alcoholism, diabetes, and congenital heart defects. Additional HF risk factors are obesity, age, reduced or falling vital capacity, smoking, and high of low hematocrit level.
- The New York Heart Association (NYHA) classification system is based largely on the assessment of symptoms.1 The new American College of Cardiology and American Heart Association (ACC/AHA) classification guidelines were designed to compliment the NYHA classification system. These new guidelines focus more on underlying disease and the need to treat early in the disease process, even before overt symptoms of heart failure are present.2
- Lifestyle changes involved in managing heart failure: Discuss diet and exercise in some detail: Staying active does not mean training as if you were going to run a marathon: but can simply mean regular walks. You can start slowly and build up under the direction of your doctor. Can reduce sodium in your diet by focusing on eating fresh meats, fruits, and vegetables; reading labels: asking questions when you eat out; and getting a low-sodium cookbook. Lifestyle changes are things you can do to influence how your feel. It may seem difficult to accomplish these things, but they are an essential part of treating heart failure. There are many resources to help you get started in incorporating these changes into your life. List any. Also, ask your friends and family for support.
- Many patients with advanced systolic heart failure exhibit significant inter- or intraventricular conduction delays that disturb the synchronous beating of the left and right ventricles so that they pump less efficiently. This delayed ventricular activation and contraction is referred to as ventricular dysynchrony and is easily recognized by a wide QRS complex on an ECG. This IVCD (inter- or intraventricular conduction delay) typically has left bundle branch morphology.
- Dr. (Name) says: Sudden Cardiac Arrest is as scary as it sounds. It means that your heart suddenly starts beating very fast and quivers instead of beating in a regular and organized way. No blood gets pumped, and you will die unless you get treatment within minutes. We’ll talk more about treatments in a moment. Unlike a heart attack, SCA is caused by an electrical problem in your heart. SCA can strike without warning, and there are no symptoms.
- Click on animation. Dr. (Name) says: Some people with Class III and IV heart failure can benefit from a heart failure pacemaker that can help your heart beat more efficiently by coordinating or synchronizing the way the heart beats, so your heart pumps more efficiently. It works by automatically checking your heart function 24 hours a day. This type of heart device is also called cardiac resynchronization therapy or CRT. You may also hear the term biventricular pacing. All refer to the same kind of treatment. Treatment with a heart device may make you feel better. Although many people experience dramatic improvements in their quality of life and in their heart failure symptoms, results may vary. Not everyone responds to the treatment in the same way. It is also important to note that heart failure pacemakers do not cure heart failure--a heart failure pacemaker is part of an overall treatment plan. Describe heart failure pacemaker device: A heart failure pacemaker is about the size of a small pocket watch that contains a battery and computer circuitry to correct your heart rhythm and help your heart beat more efficiently. Small insulated wires called leads connect the device to the heart. We’re going to pass around a plastic replica of a Medtronic combination heart failure pacemaker and defibrillator pacemaker . Facilitators circulate and pass around replicas and collect them. Before I move on, I’d like to say a few words about Medtronic, the company helping us put on the seminar today. Medtronic was the first company to introduce a pacemaker in the United States. Physicians worldwide have prescribed heart failure pacemakers for more than 120,000 patients. Other people with heart failure are in danger of having heartbeats that are irregular and/or too fast. These irregular heart beats can cause you to feel short of breath and light headed. Such episodes may also be life threatening if not treated quickly. Some heart devices also contain a defibrillator in addition to the special kind of pacemaker. This combination device also sends out small electrical signals to restore your normal heart rhythm. If the small signals do not work, the device sends out a shock to reset your heart rhythm. This kind of device is also used to treat SCA.