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Hartfalen Mortaliteit door chronisch hartfalen > 70% op 8 jaar. Harttransplant is de enige mogelijke genezing, maar < 5% van deze patiënten komen daarvoor.

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Presentatie over: "Hartfalen Mortaliteit door chronisch hartfalen > 70% op 8 jaar. Harttransplant is de enige mogelijke genezing, maar < 5% van deze patiënten komen daarvoor."— Transcript van de presentatie:

1 hartfalen Mortaliteit door chronisch hartfalen > 70% op 8 jaar. Harttransplant is de enige mogelijke genezing, maar < 5% van deze patiënten komen daarvoor in aanmerking. Palliatieve zorgen wordt bij end-stage hartfalen erg belangrijk. Symptomen/klachten van deze patiënten in eindfase (laatste weken): angst, pijn, dyspnoe, oedemen, vermoeidheid, depressie, anorexie, incontinentie, constipatie Farmacotherapie van palliatieve zorgen in deze fase omvat O 2, anxiolytica, morfine of andere narcotica, en antidepressiva, diuretica, digoxin, ACE inhibitoren, ARBs, en ß-blockers.

2 Small doses of morphine sulfate, such as 2-3 mg taken orally, may relieve dyspnea and pain. Doses may be titrated upwards as needed.

3 Drug Therapy Recommendations for Chronic HF from the 2005 ACC/AHA Guidelines Summary the importance of –risk factor modification –early detection –therapies proven to prevent and/or reduce morbidity and mortality. HF cannot be cured with drug therapy  lifelong follow-up and patient education are needed to promote adherence to diet and medications.

4

5 digoxin Sinusritme en HF: -geen impact op mortaliteit -minder HF hospitalisaties 30% (p < 0.001) goede keuze bij VKF en HF (CCB en BB in voldoende dosis vaak niet verdragen) Cave hypokaliëmie Cave nauw therapeutisch venster en interacties

6 Ambrosioni E et al. N Engl J Med 1995;332:80-85 Incidence of Death or Severe Congestive Heart Failure during Six Weeks of Treatment with Zofenopril or Placebo in Patients with Acute Myocardial Infarction

7 Ambrosioni E et al. N Engl J Med 1995;332:80-85 Cumulative Mortality during One Year of Follow-up among Patients with Acute Myocardial Infarction Treated for Six Weeks with Zofenopril or Placebo

8 Ambrosioni E et al. N Engl J Med 1995;332:80-85 Cumulative Incidence of Death from All Causes after Six Weeks of Treatment with Zofenopril or Placebo, Regardless of Whether There Was Prior Congestive Heart Failure

9 β blockers in heart failure Potential mechanisms and benefits of β blockers: improved left ventricular function; reduced sympathetic tone; improved autonomic nervous system balance; up regulation of β adrenergic receptors; reduction in arrhythmias, ischaemia, further infarction, myocardial fibrosis, and apoptosis

10 Antithrombotic treatment In patients with chronic heart failure the incidence of stroke and thromboembolism is significantly higher in the presence of atrial and left ventricular dilatation, particularly in severe left ventricular dysfunction. Nevertheless, there is conflicting evidence of benefit from routine treatment of patients with heart failure who are in sinus rhythm with antithrombotic treatment, although anticoagulation should be considered in the presence of mobile ventricular thrombus, atrial fibrillation, and severe cardiac impairment. Large scale, prospective RCT of antithrombotic treatment in heart failure are in progress, such as the WATCH study (a trial of warfarin and antiplatelet therapy); the full results are awaited with interest. The combination of atrial fibrillation and heart failure (or evidence of left ventricular systolic dysfunction on echocardiography) is associated with a particularly high risk of thromboembolism, which is reduced by long term treatment with warfarin.

11 Chronic heart failure and atrial fibrillation Restoration and long term maintenance of sinus rhythm is less successful in the presence of severe structural heart disease, particularly when the atrial fibrillation is longstanding. In patients with a deterioration in symptoms that is associated with recent onset atrial fibrillation, treatment with amiodarone increases the long term success rate of cardioversion. Digoxin is otherwise appropriate for controlling ventricular rate in most patients with heart failure and chronic atrial fibrillation, with the addition of amiodarone in resistant cases.

12 diuretica The guidelines note that periodic weight and symptom assessment should direct diuretic dosage adjustment, based on the patient's fluid status. In a nurse-driven telephone follow-up program, recently discharged HF patients were contacted at least weekly. Nurses assessed patients for symptoms of HF exacerbation and adjusted diuretic doses as appropriate. After one year, this intervention resulted in a 30% reduction in emergency department visits (p = 0.029) and readmissions (p = 0.045).[45] In another study, a patient-driven sliding-scale diuretic protocol in patients with NYHA Class II-IV HF resulted in a 90% reduction in emergency department visits (p = 0.015).[46] Diuretic dose adjustment was based on a 6 point questionnaire that evaluated signs (daily weights) and symptoms (dyspnea, peripheral edema) of HF. These data suggest that a flexible dosing strategy could enhance diuretic effectiveness.The relationship between diuretic use and the efficacy and safety of other HF therapies is also important. Symptoms of volume overload can arise upon initiation or dose escalation of a ß-blocker. Some ß-blocker clinical trials managed this complication by increasing the diuretic dose to regain a euvolemic state and improve tolerance of the increased ß-blocker dose.[40,43] Diuretic- induced volume depletion can negatively impact titration of both ACE inhibitors and ß-blockers by increasing the risk of hypotension. In the absence of fluid overload, diuretic dosage reduction should be considered.

13 Cox-inhibitoren en HF Cyclooxygenase (COX) inhibitors (both COX-2 selective and nonselective) can cause fluid retention and congestive symptoms, which may attenuate diuretic efficacy. Thus, these agents should be used cautiously or avoided entirely in HF patients. The renal effects of COX inhibitors, along with diuretic-associated volume depletion, may result in additive risks of renal dysfunction.

14 diuretica en HF Diuretic resistance may develop in -patients taking COX inhibitors -in those with significant renal impairment or excess sodium intake

15 Angor Met dank aan Professor Dr. Luc Hondeghem

16 Behoefte > Toevoer = Angor accumulatie metabolieten zuurstof tekort Definitie

17 Behoefte > Toevoer = Angor Behandeling

18 Behoefte  Stress=wandspanning volume van ventrikel R 2 druk in ventrikel wanddikte  Hartfrequentie  Contractiliteit

19 Toevoer  Bloeddruk (perfusiedruk)  Diastoleduur  Diameter (weerstand)

20 Gladde spier Contractie Relaxatie Myosin-LC Myosin-LC-PO 4 c-GMP NO Ca ++ -calmodulin Ca ++  -receptor c-AMP actin MLCK * MLCK.PO 4 i actin

21 200 ml 100 ml

22 110 ml 10 ml 100 ml

23 110 ml 10 ml100 ml 200 ml 5 ml 195 ml Dilatatie

24 110 ml 10 ml100 ml 200 ml 5 ml 195 ml Dilatatie STEAL

25 Angor  klassieke (atherosclerose).... behoefte  vasospastische (variant, Prinz-metal). vasodilatatie  onstabiele (dreigend infarct)

26 Behandeling  Nitraten   -blokkers  Calciumkanaalblokkers Behoefte Toevoer ( )

27 Nitraten  nitroglycerine ( sublinguaal, oraal, pleister/zalf ) relaxatie ( vooral veneus )... verminderde input... output kleiner hart, lagere druk maar, tachycardie (reflex) verhoogde contractiliteit  -blokkers

28 Opgepast  vers, in glazen flesje en alleen!  orthostatische hypotensie  pulserende hoofdpijn  Monday disease ( verminderde tolerantie )  Sunday disease ( afhankelijkheid )

29  Amylnitriet inhalatie Arteriële vasodilatie Venoconstriction (reflex) Corpus cavernosum

30 Ca ++ -kanaal blokkers  Phenylalkylamines (Verapamil)  Dihydropyridines (Nifedipine)  Benzothiazepines (Diltiazem)

31 Ca ++ -Kanaal N D+ V- Inactivation Activation Selectivity HOOC H2NH2N

32 Weefselspecificiteit Ca ++ Receptor operated L-type (voltage operated) N T-

33 Relaxatie  bloedvaten (N,D,V) vooral arteriolen (oedeem vnl. door extravasatie) minder venen (geen orthostatische hypotensie)  hart (D,V) (N heeft al perifere effecten bij dosis die nog geen cardiaal effect heeft) SA, AVB, CHF  skeletspieren 0  bronchi, GI (constipatie)

34 Angor  vasodilatatie... verlaagde bloeddruk  contractiliteit  hartfrequentie (  N, ~ D,  V)  coronaire spasmen (vasosp. angor)

35 angor acute aanvalonderhoudstherapie Organische nitraten ++ CCB (+)+ β-blockers -+

36 Eerste (thuis)behandeling bij klinisch vermoeden van acuut myocardinfarct: 300 mg (snel resorbeerbaar) ASA po nitraten SL (niet teveel) morfine iv of sc (niet im)

37 Cumulative Mortality Rate Years to Death Cumulative Event Rates for All-Cause Mortality by ALLHAT Treatment Group HR (95% CI)p value A/C0.96 ( )0.20 L/C1.00 ( )0.90 ALLHAT Chlorthalidone Amlodipine Lisinopril

38 Cumulative Mortality Rate Years to Death Cumulative Event Rates for All-Cause Mortality by ALLHAT Treatment Group HR (95% CI)p value A/C0.96 ( )0.20 L/C1.00 ( )0.90 ALLHAT Chlorthalidone Amlodipine Lisinopril


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