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Don’t Forget لا تنسوا أقصانا. Prof. A. ABU-HASHEM (M.D. Cardiology) Zagazig, Egypt.

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Presentation on theme: "Don’t Forget لا تنسوا أقصانا. Prof. A. ABU-HASHEM (M.D. Cardiology) Zagazig, Egypt."— Presentation transcript:

1 Don’t Forget لا تنسوا أقصانا

2 Prof. A. ABU-HASHEM (M.D. Cardiology) Zagazig, Egypt

3 “In these hearts …… their reserve force lost and with it the power of meeting the demands in maintaining the circulation during severe exertion”……. (Osler, 1892). (Osler, 1892).

4 “ A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with requirements of the metabolizing tissues” (Braunlwald, 1986). (Braunlwald, 1986).

5 Most cases of CHF respond favorably to pharmaco and non-pharmaco therapies. Some do not improve or suffered from rapid recurrence despite optimal therapy and have symptoms at rest or minimal exertion, can not perform daily activities, frequently suffering from anasarca and cachexia and require repeated hospitalization; Refractory HF.

6 EPIDEMIOLOGY CHF is major cause of mortality and morbidity especially among elderly and is considered a serious health problem. CHF is major cause of mortality and morbidity especially among elderly and is considered a serious health problem. 4-7 million is USA have CHF. 4-7 million is USA have CHF. 400,000 new cases every year. 400,000 new cases every year. CHF is the 1ry cause of death in 40,000 / year. CHF is the 1ry cause of death in 40,000 / year. CHF is the most frequent cause of hospitalization in medicare population. CHF is the most frequent cause of hospitalization in medicare population.

7 RHF accounts for 5% of symptomatic HF. Incidence of RHF increases with age and is more in males. Risk of death in mild CHF is 5-10% annually. This increases much in RHF up to 50%. EPIDEMIOLOGY

8 The burden associated with RHF is expected to increase due to : I.Ageing of the population. II.Increase numbers of elderly with CAD and HPN. III.Improved diagnosis e.g echo. EPIDEMIOLOGY

9 ETIOLOGY Ischemic (extensive CAD, multiple MI). Non-ischemic CM (younger, some with family history). Hypertension.Valvular. Viral myocarditis.

10 Precipitating (Aggravating) Factors. 1.Cardiac : arrhythmias, M.I. 2.Non cardiac : anemia, pul.embolism, infections, other illness. 3.Treatment-related: poor compliance, NSAID, steroids, B.B.

11 The vicious circle of pathophysiology Chamber dilatation Vent- Dysfunction Wall stress Renal Vasoconstriction H 2 o and Na retention Toxic effects (Apoptosis, myocyte loss) Vasoconstriction (afterload)  HR, Arrhythmia Neuro- hormones

12 Vent. Remodeling Vent. Remodeling More functional deterioration Changes in geometry ( from prolate ellipse to more spherical shape), volume and architexture Impairment of skeletal muscle metabolism.  TNF… muscle atrophy. Resulting in cachexia, and exercise intolerance Changes is the biology and volume of myocytes and non-myoctes components of the myocardium

13 Symptoms of RHF 1.Dyspnea III or IV. 2.Orthopnea,PND,exertional and nocturnal dry cough. 3.Fatigue, weakness. 4.Dizzy spells or palpitations due to frequent tachyarrhythmias. 5.Fluid retentions, LL edema, ascites….

14 Physical exam. 1.Increased JVP with prominent V-wave. 2.Generalized anasarca. 3.Cardiac dilatation, galloping and murmurs. 4.Fine lung crepitations. 5. Tender hepatomegaly.

15 Functional evaluation 1.NYHA classification (insensitive, subjective) 2.Six-minute walk (<305 met. in 6 min.  bad prognosis). 3.Peak maximal oxygen utilization (MVO 2 < 10 ml/kg/min in high risk pt.). 4.Exercise testing: modified Bruce or Naughton protocols (reduced speeds and slow increments). 5.Metabolic equivalents and work capacity (METs) are reduced.

16 Diagnostic investigations 1.Confirm the clinical diagnosis. 2.Identify an underlying causes. 3.Identify precipitating factors. 4.Guide therapy. 5.Determine prognosis.

17 ECG Nonspecific ST- T changes. Chambers enlargement. Old MI. BBB and other conduction defects. Tachyarrhythmias: AF, A fl, VPCs, VT….

18 Chest x-ray Upper lobe congestion. Interstitial edema. Kerley’s A and B lines. Pleural effusions.




22 Echo Doppler Dimensions, volumes, wall thickness. Function: EF, FS, diastolic dysfunction. Valvular structure and function. Pressures: m PAP, RVSP. Spont. echo contrast, masses, thrombi. Pericardial diseases.

23 TEE Inadequate TTE. Suspected IE. Prosthetic valve function LAA thrombi.


25 Echo (cont.) DSE: at low dose for detection of viable myocardium. DSE: at low dose for detection of viable myocardium. Myocardial tissue contrast: to detect ischemia and viability. Myocardial tissue contrast: to detect ischemia and viability.

26 Radionuclide scintigraphy Non diagnostic echo study RV functions Viable myocardium PET is more sensitive than Thallium- 201 study.


28 Cardiac magnetic resonance The most accurate for volumes, thickness and masses. Detection of myocardial necrosis, perfusion and function. Quantitative biochemical information: myocardial energetics.


30 Other tests Routine laboratory:  ESR, anemia,  serum iron, thrombocytopenia. Electrolyte: Na +, k +, Mg ++. Liver and kidney function tests. Thyroid function.

31 Viral study (serum or myocardial biopsy). Serum ANP or urinary proatrial natriuretic peptide (N-ANP) or (N-BNP). Spirometry and respiratory function tests in selected cases. Other tests

32 Invasive tests Usually not required, but may be needed to elucidate the cause of RHF. Usually not required, but may be needed to elucidate the cause of RHF. Coronary angiography. Coronary angiography. Hemodynamic monitoring. Hemodynamic monitoring. Endomyocardial biopsy. Endomyocardial biopsy.

33 Diagnostic criteria of RHF Major : 1.Resting LVEF < 30%. 2.NYHA III or IV. 3.Peak VO 2 <14ml/kg/min on symptom limited testing (4-5 METs).

34 Minor : 1.No or minimal response after at least 3m of full standard therapy (ACEI,digoxin, diuretics). 2.Serum Na < 130 mq./L. in pt. not treated with ACEIs. 3.Plasma norepinephrine > 900 pg/ml. Contributing : 1.More than one hospitalization for worsening HF in the past 6 ms. 2.Cardiac cachexia. Diagnostic criteria of RHF

35 Management of RHF Prevention of RHF The basic aims of prevention are to : Limit myocardial damage. Modulate and reduce neuroendocrine activation. Modulate and reduce neuroendocrine activation. This includes : Treatment of risk factors (smoking/ lipids/ HPN…). Revascularization for cases with significant reversible ischemia.

36 Life style modification Life style modification Diet : small meals, less fat, high fiber diet. Diet : small meals, less fat, high fiber diet. Limited dietary sodium  2 gm/day. Limited dietary sodium  2 gm/day. Reduced fluid intake. Reduced fluid intake. Avoidance of traveling to high altitude, very hot or humid places. Short air flights are preferred to other means of transport. Avoidance of traveling to high altitude, very hot or humid places. Short air flights are preferred to other means of transport. Management of RHF

37 Non pharmacological therapy 1.Exercise and rehabilitation : Regular physical activity is recommended according to the patient’s condition. Walking or cycling for 10-30 min/day 3- 7d/w. Moderate – intensity resistance training improves strength, endurance, HR variability, and forearm blood flow.

38 2.Rest: Necessary in severe RHF. Passive mobilization and respiratory exercise are advised. 3.Education of the patient and relatives about disease condition, life style modification,drug side effects. Non pharmacological therapy

39 Specific pharmacological therapy Diuretics Loop diuretics, thiazides and potassium sparing. RALES mortality study : (low dose spironolactone + ACEIs + loop diuretics) markedly and progressively improved survival in RHF irrespective of etiology.

40 Treatment of diuretics resistance : Fluid restriction. Fluid restriction. Change the route (oral to i.v.) and timing (single multiple & continuous infusion) Change the route (oral to i.v.) and timing (single multiple & continuous infusion) Combination therapy (Furosemide. HCZ) Combination therapy (Furosemide. HCZ)

41 Furosemide + HSS High dose Furosemide (i.v. infusion for 500- 1000 mg) plus hypertonic saline solution (150 ml 1.4-4.6% NaCl) bid in 30 min for 6-12 days. Improved clinical and hemodynamic parameters, reduced hospitalization, and maintained the obtained results over time in comparison with the use of high dose Furosemide as bolus.

42 ACEIs Start with small doses with gradual increments. Regular check up of renal function and K +. Significantly improved survival and reduce hospitalization. Many trials (SOLVD, SAVE, PROMISE, PROVED,…)

43 Dry cough, hypotension,  K +, renal insufficiency are side effects. ARBS: are the best substitute in the presence of side effects (CHARM study). Combination therapy remains to be defined (ON TARGET). ACEIs


45 Vasodilators Isosorbide dinitrate and hydralazine in combination in V-HeFT trial yield significant survival benefit in comparison to placebo and prazocin.

46 Digitalis Routine for CHF and AF. In SR : debates regarding its beneficial effects vs toxic effects( DIG trial). Smaller doses, in elderly, renal or hepatic insufficiency. Serum digoxin levels and electrolyte check up.

47  Dobutamine, Dopamine and Milrinone.  The routine use in RHF is not recommended.  Best indicated in: acute HF, bridge to definitive treat. (revascularization or transplantation) or palliation in end stage RHF. Inotropes

48 Combination of B-blockers and phosphodiesterase inhibitors (milrinone and enoximone) seems to be beneficial, with less side effects. Inotropes

49 B- Blockers HF is associated with enhanced adrenergic activity with its direct and indirect toxic myocardial effects. B-B is indicated in mild-moderate HF pretreated with standard therapy. CAPRICORN study using Carvedilol and MERIT heart failure trial using Metoprolol, showed reduction in total mortality by 34% and SCD by 41%.

50 However, symptomatic benefit may be delayed and initial worsening may occur. It is an important issue in decision making about starting B.B in severely symptomatic cases. B- Blockers


52 Antithrombotics RHF is associated with increased risk of thromboembolism. The annual risk of stroke in controlled CHF is 1-2%. In stroke prevention in AF (SPAF), it was 10.3% in chronic and 17.7% recent CHF.

53 Anticoagulants definitely reduced risk of stroke in the presence of AF, while this not yet proved in SR. Intracardiac thrombi and probably SEC are strong indications for long term oral anticoagulants. Antithrombotics

54 Antiarrhythmics A.For SVT: AF, flutter, SVT. 1.Digoxin to control vent.rate at rest only. 2.B-blockers: to control vent.rate during exercise. 3.Amiodarone if B-B are contraindicated. 4.AVN ablation, AF ablation(PV isolation) in refractory cases.

55 B.For vent tachy.: non sust.VT,sust.VT, SCD. 1.B-blockers. 2.Amiodarone. 3.ICD. 4.Radiofrequency ablation (not yet of proven efficacy) Antiarrhythmics


57 Statins in CHF Among the cholesterol – independed effects of statins is the antihypertrophic on the heart Limited studies showed that statins improved the quality of life and exercise capacity in patient with nonischemic CM. Thus statins may be a promising novel treatment strategy in RHF.

58 Drugs under investigations 1. Vasopeptidase inhibitors (Omapatrilat) Block not only ACE but also neutral endopeptidase which leads to enhanced activity of endogenous vasodilators (ANP). Used in HPN and CHF. In a small scale study they improved morbidity and mortality in RHF. May be superior to ACEIs.

59 2. Cytokine antagonists (TNF antagonists): Etanercept or Infliximab. In a short term pilot study Etanercept in CHF showed improvement in clinical status and  EF and  LV size. Drugs under investigations

60 3. Endothelin antagonists: Serum endothelin-1 is elevated in RHF. It has a potent vasoconstrictive action with adverse effects in the structure and function of the heart and peripheral vessels. Bosentan in a small dose is an endothelin receptor antagonist, with promising initial results in a large-scale ongoing study. Drugs under investigations

61 Future prospects New methods to promote angiogenesis (gene therapy), stem cell implantation and autogenous myocyte cultures. Given intracoronary or intrapericardial hoping to increase vascularity and hence viability and function of the myocardium.

62 Ultrafilteration Is employed in resistant cases with fluid retention. To remove excess water and sodium, thus escape from the cardiorenal vicious circle. Intermittent hemofilteration and hemodialysis. More effectively using extracorporeal or slow isolated ultrafilteration.

63 Pacemakers is RHF Resynchronization therapy Based on the presence of intravent. conduction disturbance resulting in discoordinated vent.conduction in 30% of CHF. Resynchronization using biventricular or multisites pacing, enhances vent. contraction and reduces MR. Although complex procedure, marked improvement in symptoms and exercise tolerance is achieved (MUSTIC study).

64 LV assist Devices Used as a temporary bridge to cardiac transplantation or recovery of the heart post-cardiac surgery or from a major cardiac insult.

65 Biomechanical assistance of LV and / or RV can be achieved with a variety of devices ranging from enhanced external counter pulsation (EECP), IABC to Vent. Assist systems and to totally implantable artificial heart. LV assist Devices

66 Surgery for RHF 1.Revascularization in IHD with viable myocardium: CABG or transmural laser revascularization (TLR). 2.Mitral reconstruction (MVR or replacement) in severe MR, with excellent short and intermediate term outcome. 3.Aneurysmectomy.

67 4.Cardiomyoplasty via stimulated skeletal muscle wraps and recently via nonstimulated synthetic wraps. 5.Partial left ventriculectomy (Batista) in trial to restore normal cardiac dimensional physiology. Surgery for RHF

68 5. Cardiac transplantation : Indications : NYHA IV, VO 2 max < 10 ml /kg/min Recurrent uncontrolled VT.. Severe ischemia not amenable to revascularization. EF < 20%. Contraindications : Age > 65 years old. Active infections, malignancy, DM, renal or hepatic failure. Fixed severe PH. Surgery for RHF

69 Although cardiac transplantation is the most effective therapy for end-stage RHF, yet it is limited by donor organ supply and need for immunosuppression. Xenotransplantation: especially porcine or non human primate hearts may represent a solution to the organ shortage. Surgery for RHF


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