Congestive Heart Failure

Congestive Heart Failure,

Prepared By Dr.Mustafa AlshehabatTerminologyHeart Failure: The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body.Pulmonary Edema: An abnormal accumulation of fluid in the lungs.CHF with Acute Pulmonary Edema: Pulmonary Edema due to Heart Failure (Cardiogenic Pulmonary Edema)What is HFComplex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation. PathophysiologyMain Causes of Heart Failure: Ischemic Heart Disease (35-40%) Cardiomyopathy(dilated) (30-34%) Hypertension (15-20%) Other Causes: Valvular Heart Disease. Congenital Heart Disease. Alcohol and Drugs. Arrhythmias

Pathophysiological Changes in HFVentricular Dilatation.Myocyte Hypertrophy.Salt and Water Retention.Sympathetic Stimulation.Peripheral Vasoconstriction.

Signs & Symptoms Symptoms:Exertional DyspnoeaOrthopniaParaxysmal Nocturnal Dyspnoea

Signs: CardiomegalyElevated Jugular Venous PressureTachycardiaHypotensionBi-basal cracklesPleural effusionAnkle EdemaAscitesTender hepatomegaly.

Classification of heart failureNo limitation. Normal physical exercise doesnt cause fatigue, dyspnea or palpitations.Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnea or palpitations.Marked limitation. Comfortable at rest but gentle physical activity produces marked symptoms of HF.Symptoms of HF occur at rest and are exacerbated by any physical activity.Kussmauls Sign

This is a rise in the JVP seen with inspiration. It is the opposite of what is seen in normal people and this reflects the inability of the heart to compensate for a modest increase in venous return. This sign is classically seen in constrictive pericarditis in association with a raised JVP. This condition was originally described in tuberculous pericarditis and is rarely seen. Kussmauls sign is also seen in right ventricular infarction, right heart failure, tricuspid stenosis, and restrictive cardiomyopathy. It is not seen in acute cardiac tamponade- although it may be seen if tamponade occurs with a degree of constricive pericardiditisPMIThe apex beat, also called the point of maximum impulse (PMI), is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt. The cardiac impulse is the result of the heart rotating, moving forward and striking against the chest wall during systole.The normal apex beat can be palpated in the precordium left 5th intercostal space, at the point of intersection with the left midclavicular line. In children the apex beat occurs in the fourth rib interspace medial to the nipple. The apex beat may also be found at abnormal locations; in many cases of dextrocardia, the apex beat may be felt on the right side. Lateral and/or inferior displacement of the apex beat usually indicates enlargement of the heart.

Heart Sounds

S1The first heart sound - S1 - is in time with the pulse in your carotid artery in your neck. The sound of the tricuspid valve closing may be louder in patients with pulmonary hypertension due to increased pressure beyond the valve. Non-heart-related factors such as obesity, muscularity, emphysema, and fluid around the heart can reduce both S1 and S2.The position of the valves when the ventricles contract can have a big effect on the first heart sound. If the valves are wide open when the ventricule contracts, a loud S1 is heard. This can occur with anemia, fever or hyperthyroid.When the valves are partly closed when the ventricule contracts, S1 is faint. Beta-blockers produce a fainter S1. Structural changes in the heart valves can also affect S1. Fibrosis and calcification of the mitral valve may reduce S1, while stenosis of the mitral valve may cause a louder S1.S2The second heart sound marks the beginning of diastole - the heart's relaxation phase - when the ventricles fill with blood. In children and teenagers, S2 may be more pronounced. Right ventricular ejection time is slightly longer than left ventricular ejection time. As a result, the pulmonic valve closes a little later than the aortic valve.Higher closing pressures occur in patients with chronic high blood pressure, pulmonary hypertension, or during exercise or excitement. This results in a louder A2 (the closing sound of the aortic valve).On the other hand, low blood pressure reduces the sound. The second heart sound may be "split" in patients with right bundle branch block, which results in delayed pulmonic valve closing. Left bundle branch block may cause aortic valve closing (A2) to be slower than pulmonic valve closing (P2).S3During diastole there are 2 sounds of ventricular filling: The first is from the atrial walls and the second is from the contraction of the atriums. The third heart sound is caused by vibration of the ventricular walls, resulting from the first rapid filling so it is heard just after S2. The third heart sound is low in frequency and intensity. An S3 is commonly heard in children and young adults. In older adults and the elderly with heart disease, an S3 often means heart failure.S4The fourth heart sound occurs during the second phase of ventricular filling: when the atriums contract just before S1. As with S3, the fourth heart sound is thought to be caused by the vibration of valves, supporting structures, and the ventricular walls. An abnormal S4 is heard in people with conditions that increase resistance to ventricular filling, such as a weak left ventricle.

EdemaBilateral lower extremity edemaHypertensionHypertrophic Cardiomyopathy

Compensatory MechanismsIncreased Heart RateSympathetic = Norepinephrine

DilationFrank Starling = Contractility

NeurohormonalRedistribution of Blood to the BrainCHF Vicious CycleLow Output

Increased Preload Increased AfterloadNorepinephrine

Increased SaltVasoconstrictionRenal Blood Flow

ReninAngiotension IAngiotension IIAldosterone Infiltration of Interstitial SpaceNormal Micro-anatomy

Micro-anatomy with fluid movement.

Acute Pulmonary Edema a true life- threatening emergency

Treatment Prevention. Control of risk factors Life style Treat etiologic cause / aggravating factors Drug therapy Personal care. Team work Revascularization if ischemia causes HF ICD (Implantable Cardiac Defibrillator) Ventricular resyncronization Ventricular assist devices Heart transplant Artificial heart Neoangiogenesis, Gene therapyAllSelected patients18 Treatment ObjectivesSurvivalMorbidityExercise capacityQuality of lifeNeurohormonal changes Progression of CHFSymptoms(Cost)19Treatment of Heart Failure.ObjectivesThe objectives of treatment of the patient with heart failure are many, but they may be summarized in two principles: decrease symptoms and prolong life. In daily practice, the first priority is symptom control and the best plan is to adjust to the individual patients particular circumstances over the course of therapy. Nevertheless, the rest of the listed objectives should not be forgotten, as medical therapy now has the potential for decreasing morbidity (hospital admissions, embolism, etc.), increasing exercise capacity (all of the usually prescribed drugs), improve the quality of life, control neurohormonal changes (ACE-I, beta blockers), retard progression (ACEI) and prolong life.

TreatmentPharmacologic TherapyDiureticsACE inhibitorsBeta BlockersDigitalisSpironolactoneOther20Treatment of Heart Failure.DrugsThis is a simple and pragmatic classification of the vast numbers and types of medications in the pharmacopoeia for the treatment of heart failure.Diuretics Essential to control symptomssecondary to fluid retention Prevent progression from HT to HF Spironolactone improves survival New research in progress21

CortexMedullaThiazidesInhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of HenleK-sparingInhibit reabsorption of Na in thedistal convoluted and collecting tubuleLoop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of HenleLoop of HenleCollecting tubuleDiuretics22Treatment of heart failure.Diuretics: Classification and mechanisms of action

Diuretics are drugs which eliminate Na and water by acting directly on the kidney. This category does not include other drugs with principle actions different from the diuretics, but which increase diuresis by improving heart failure or by mechanisms on the kidney which are incompletely understood. The diuretics are the primary line of therapy for the majority of patients with heart failure and pulmonary congestion. Diuretics (loop, thiazides and potassium-sparing) produce a net loss of Na and water acting directly on the kidney, decrease acute symptoms which result from fluid retention (dyspnea, edema). Diuretic drugs are classically divided into three groups: 1) thiazides, 2) loop diuretics and 3) potassium-sparing. Thiazide diuretics inhibit the active transport of Cl-Na in the cortical diluting segment of the ascending limb of the Loop of Henle.Loop diuretics inhibit the transport of Cl-Na-K in the thick portion of the ascending limb of the Loop of Henle.Potassium-sparing diuretics inhibit the reabsorption of Na in the distal convoluted and collecting tubules.Diuretics. Indications1.Symptomatic HF, with fluid retention Edema Dyspnea Lung Rales Jugular distension Hepatomegaly Pulmonary edema (Xray)AHA / ACC HF guidelines 2001 ESC HF guidelines 20012311Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weightMonitor serum K+ at frequent intervalsReduce dose when fluid retention is controlledTeach the patient when, how to change doseCombine to overcome resistanceDo not use alone24Loop diuretics. Dose (mg) InitialMaximumBumetanide 0.5 to 1.0 / 12-24h 10 / dayFurosemide 20 to 40 / 12-24h 400 / dayTorsemide 10 to 20 / 12-24h 200 / dayAHA / ACC HF guidelines 2001 25Thiazides, Loop Diuretics. Adverse Effects K+, Mg+ (15 - 60%) (sudden death ???) Na+ Stimulation of neurohormonal activity Hyperuricemia (15 - 40%) Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic

Sharpe N. Heart failure. Martin Dunitz 2000;43Kubo SH , et al. Am J Cardiol 1987;60:1322MRFIT, JAMA 1982;248:1465Pool Wilson. Heart failure. Churchill Livinston 1997;63526 VASOCONSTRICTIONVASODILATATION KininogenKallikreinInactive FragmentsAngiotensinogenAngiotensin IRENINKininase IIInhibitorALDOSTERONESYMPATHETICVASOPRESSINPROSTAGLANDINStPAANGIOTENSIN IIBRADYKININACE-i. Mechanism of ActionA.C.E.27Treatment of Heart FailureAngiotensin Converting-Enzyme Inhibitors (ACEI) :Mechanisms of actionACE-inhibitors competitively block the converting enzyme that transforms angiotensin I into angiotensin II. The reduction in angiotensin II levels explains its arteriovenous vasodilatory actions, as angiotensin II is a potent vasoconstrictor that augments sympathetic tone in the arteriovenous system. Additionally, angiotensin causes vasopressin release and produces sodium and water retention, both through a direct renal effect and through the liberation of aldosterone. Since converting enzyme has a similar structure to kinase II that degrades bradykinin, ACE-inhibitors increase kinin levels that are potent vasodilators (E2 and F2) and increase release of fibrinolytic substances such as tPA.ACE-I. Clinical Effects Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival28Treatment of Heart Failure.Angiotensin Converting-Enzyme Inhibitors (ACEI): Mechanisms of actionACE-inhibitors cause arteriovenous vasodilatation. Venodilation is accompanied by reduction in PAD, PCWP, and LVEDP. Arterial vasodilatation decreases SVR and MAP and increases cardiac output, ejection fraction, and exercise tolerance. Heart rate and contractility do not change, and, thus, double product and myocardial oxygen demand are decreased. These effects are more noticeable in patients with low sodium levels, in whom there is an increased plasma renin activity. Vasodilatation is seen in various vascular territories: renal, coronary, cerebral, and musculoskeletal (increasing exercise capacity). Additionally, ACE-inhibitors cause diuretic and natriuretic effects that are a consequence of the inhibition of angiotensin II and aldosterone synthesis, as well as the increase in cardiac output and renal perfusion. It is now known that the magnitude and duration of blood pressure reduction correlates better with the activity of ACE in certain tissues (heart, vessels, kidney, adrenal, etc.) than with its plasma levels, which indicates that ACE-inhibitors act by inhibiting local tissue production of angiotensin II. Plasma levels of ACE are not good predictors of the magnitude of hemodynamic effects of ACE-inhibition.

Symptomatic heart failure

Asymptomatic ventricular dysfunction- LVEF < 35 - 40 %

Selected high risk subgroupsACE-i. IndicationsAHA / ACC HF guidelines 2001 ESC HF guidelines 200129Treatment of Heart FailureAngiotensin Converting-Enzyme Inhibits (ACEI) Indications.ACE-inhibitors probably constitute the cornerstone of drug therapy for heart failure, in that administration over time leads to amelioration of symptoms, beneficial hemodynamic changes, increased functional capacity, regression of structural changes, and, unequivocally, prolongation of survival. Thus, ACE-inhibitors are first-line therapy, not only in symptomatic heart failure patients, but also in patients with asymptomatic left ventricular dysfunction. The exact degree of ventricular dysfunction below which it is advisable to begin therapy with an ACE-inhibitor has not been defined; however, in general terms they can be helpful in patients with ejection fractions less than 35%.ACE-I. Adverse EffectsHypotension (1st dose effect)Worsening renal functionHyperkalemiaCoughAngioedemaRash, ageusia, neutropenia, 30Treatment of Heart Failure.Angiotensin Converting-Enzyme Inhibitors (ACEI) : Undesirable EffectsThese can be classified into two groups. One group includes those effects that are inherent to its mechanism of action, and therefore are common to all ACE-inhibitors. The other includes those effects that are related to the specific chemical structure of the drug. In this case, substitution of one ACE-inhibitor for another could possibly reduce the intensity of the adverse reaction (e.g. choosing an ACE-inhibitor without a sulfhydryl moiety).ACE-I. Contraindications Intolerance (angioedema, anuric renal fail.) Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl) Hyperkalemia (> 5,5 mmol/l) Severe hypotension31Treatment of Heart FailureAngiotensin Converting-Enzyme Inhibitors (ACEI) Contraindications.There are few absolute contraindications for the use of ACE-inhibitors. The most important one is the presence of renal artery stenosis. The most frequent contraindication is intolerance of the drug. Hypotension, the presence of renal insufficiency, or hyperkalemia limits their use, or the ability to administer adequate doses, in up to 20% of patients.-Adrenergic BlockersMechanism of action Density of 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HRAntiischemicAntihypertensiveAntiarrhythmicAntioxidant, Antiproliferative32Treatment of congestive heart failure.Possible benefits of beta adrenergic blockers

The use of -blockers in patients with heart failure is controversial. Nevertheless, this slide lists some of the potentially beneficial effects of these drugs for patients in heart failure.

-Adrenergic BlockersClinical Effects Improve symptoms (only long term) Reduce remodelling / progression Reduce hospitalization Reduce sudden death Improve survival33Treatment of Heart Failure.Angiotensin Converting-Enzyme Inhibitors (ACEI): Mechanisms of actionACE-inhibitors cause arteriovenous vasodilatation. Venodilation is accompanied by reduction in PAD, PCWP, and LVEDP. Arterial vasodilatation decreases SVR and MAP and increases cardiac output, ejection fraction, and exercise tolerance. Heart rate and contractility do not change, and, thus, double product and myocardial oxygen demand are decreased. These effects are more noticeable in patients with low sodium levels, in whom there is an increased plasma renin activity. Vasodilatation is seen in various vascular territories: renal, coronary, cerebral, and musculoskeletal (increasing exercise capacity). Additionally, ACE-inhibitors cause diuretic and natriuretic effects that are a consequence of the inhibition of angiotensin II and aldosterone synthesis, as well as the increase in cardiac output and renal perfusion. It is now known that the magnitude and duration of blood pressure reduction correlates better with the activity of ACE in certain tissues (heart, vessels, kidney, adrenal, etc.) than with its plasma levels, which indicates that ACE-inhibitors act by inhibiting local tissue production of angiotensin II. Plasma levels of ACE are not good predictors of the magnitude of hemodynamic effects of ACE-inhibition.

Symptomatic heart failure

Asymptomatic ventricular dysfunction- LVEF < 35 - 40 %

After AMIAHA / ACC HF guidelines 2001 ESC HF guidelines 2001-Adrenergic BlockersIndications34Treatment of Heart FailureAngiotensin Converting-Enzyme Inhibits (ACEI) Indications.ACE-inhibitors probably constitute the cornerstone of drug therapy for heart failure, in that administration over time leads to amelioration of symptoms, beneficial hemodynamic changes, increased functional capacity, regression of structural changes, and, unequivocally, prolongation of survival. Thus, ACE-inhibitors are first-line therapy, not only in symptomatic heart failure patients, but also in patients with asymptomatic left ventricular dysfunction. The exact degree of ventricular dysfunction below which it is advisable to begin therapy with an ACE-inhibitor has not been defined; however, in general terms they can be helpful in patients with ejection fractions less than 35%.HypotensionFluid retention / worsening heart failureFatigueBradycardia / heart block-Adrenergic BlockersAdverse EffectsReview treatment (+/-diuretics, other drugs)Reduce doseConsider cardiac pacingDiscontinue beta blocker only in severe cases35Na+K+K+Na+Na+Ca++Ca++Na-K ATPaseNa-Ca ExchangeMyofilamentsDigitalisCONTRACTILITY

-36Treatment of heart failure.Digoxin: Mechanism of action

Digoxin attaches to specific receptors which form a part of the enzyme, Na+/K+-dependent ATP-ase (sodium pump), inhibiting it. This blockade produces a progressive increase in the intracellular concentration of Na, which in turn activates the exchange of Na+-Ca++ and increases the influx of Ca++ and its intracellular concentration, [Ca++]i. This increase in the [Ca++]i at the level of the contractile proteins explains the resultant increase in cardiac contractility.Digitalis. Mechanism of ActionBlocks Na+ / K+ ATPase => Ca+ +Inotropic effectNatriuresisNeurohormonal control- Plasma Noradrenaline- Peripheral nervous system activity- RAAS activity - Vagal tone- Normalizes arterial baroreceptorsNEJM 1988;318:358 37Digitalis. Clinical Effects Improve symptoms Modest reduction in hospitalization Does not improve survival38Treatment of Heart Failure.Angiotensin Converting-Enzyme Inhibitors (ACEI): Mechanisms of actionACE-inhibitors cause arteriovenous vasodilatation. Venodilation is accompanied by reduction in PAD, PCWP, and LVEDP. Arterial vasodilatation decreases SVR and MAP and increases cardiac output, ejection fraction, and exercise tolerance. Heart rate and contractility do not change, and, thus, double product and myocardial oxygen demand are decreased. These effects are more noticeable in patients with low sodium levels, in whom there is an increased plasma renin activity. Vasodilatation is seen in various vascular territories: renal, coronary, cerebral, and musculoskeletal (increasing exercise capacity). Additionally, ACE-inhibitors cause diuretic and natriuretic effects that are a consequence of the inhibition of angiotensin II and aldosterone synthesis, as well as the increase in cardiac output and renal perfusion. It is now known that the magnitude and duration of blood pressure reduction correlates better with the activity of ACE in certain tissues (heart, vessels, kidney, adrenal, etc.) than with its plasma levels, which indicates that ACE-inhibitors act by inhibiting local tissue production of angiotensin II. Plasma levels of ACE are not good predictors of the magnitude of hemodynamic effects of ACE-inhibition.

Digitalis. Indications When no adequate response to ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001 In combination with ACE-i + diuretics if persisting symptoms ESC Guidelines 2001 AF, to slow AV conduction

Dose 0.125 to 0.250 mg / day39 ALDOSTERONE Retention Na+ Retention H2O

Excretion K+ Excretion Mg2+ Collagen deposition

Fibrosis - myocardium - vesselsSpironolactone Edema ArrhythmiasCompetitive antagonist of thealdosterone receptor(myocardium, arterial walls, kidney)Aldosterone Inhibitors-40Treatment of congestive heart failure.Aldosterone inhibitors: Mechanism of action

Aldosterone acts directly on specific receptors. At the renal level it produces retention of sodium and water, resulting in an increase in preload and afterload, edema formation and the appearance of symptoms of pulmonary and systemic venous congestion. In addition, it increases the elimination of potassium and magnesium, creating an electrolyte imbalance which may be responsible in part for cardiac arrhythmias. At the tissue level, aldosterone stimulates the production of collagen, being in large part responsible for the fibrosis that is found in hypertrophied myocardium and in the arterial walls of patients with heart failure. The beneficial effects of spironolactone derive from the direct and competitive blockade of specific aldosterone receptors. Aldosterone inhibitors therefore have three types of effects:- Diuretic effect, which is most noticeable when fluid retention and increased levels of aldosterone are present.- Antiarrhythmic effect, mediated by the correction of hypokalemia and hypomagnesemia.- Antifibrotic effect. This effect, demonstrated in animal models, can contribute to a decrease in the progression of structural changes in patients with heart failure.Spironolactone. Practical use Do not use if hyperkalemia, renal insuf.Monitor serum K+ at frequent intervalsStart ACE-i firstStart with 25 mg / 24hIf K+ >5.5 mmol/L, reduce to 25 mg / 48hIf K+ is low or stable consider 50 mg / day New studies in progress41 RENINAngiotensinogenAngiotensin I

ANGIOTENSIN II

ACEOther pathwaysVasoconstrictionProliferative Action

Vasodilatation Antiproliferative Action

AT1 AT2AT1 Receptor Blockers

RECEPTORSAngiotensin II Receptor Blockers (ARB)42Treatment of congestive heart failure.Angiotensin II inhibitors

Angiotensin II has different effects mediated via specific receptors. There are two types of tissue receptors for angiotensin: AT1 and AT2. Stimulation of AT1 receptors has a proliferative and vasoconstrictor effect, while stimulation of AT2 receptors has the opposite effects, that is, vasodilatory and antiproliferative. In the treatment of heart failure, specific blockade of the AT1 receptors is desirable. Drugs which create a selective and competitive block of the AT1 receptors include:losartan, valsartan, irbersartan and candersartan. 1- VENOUS VASODILATATION Preload

2- Coronary vasodilatation Myocardial perfusion

3- Arterial vasodilatation Afterload

4- OthersPulmonary congestionVentricular sizeVent. Wall stressMVO2NITRATESHEMODYNAMIC EFFECTS Cardiac output Blood pressure43Treatment of Heart Failure.Nitrates: Hemodynamic effectsAt therapeutic doses, nitrates produce venodilatation that reduces systemic and pulmonary venous resistances. As a consequence, right atrial pressure, pulmonary capillary pressure, and LVEDP decrease. The preload reduction improves the signs of pulmonary congestion and decreases myocardial wall tension and ventricular size, which in turn reduce oxygen consumption. With higher doses, nitrates produce arterial vasodilatation that decreases peripheral vascular resistance and mean arterial pressure, leading to a decrease in afterload, and thereby reduce oxygen consumption. This arterial vasodilatation increases cardiac output, counteracting the possible reduction caused by the reduction in preload caused by venodilatation. The overall effect on cardiac output depends on the LVEDP; when LVEDP is high, nitrates increase cardiac output, while when it is normal nitrates can decrease cardiac output. Nitrates can also produce coronary vasodilatation, as much through reducing preload as through a direct effect on the vascular endothelium. This vasodilatation can decrease the mechanical compression of subendocardial vessels and increases blood flow at this level. Additionally, nitrates reduce coronary vascular tone, overcoming vasospasm.Nitrates. Clinical UseCHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspneaIn acute CHF and pulmonary edema:NTG sl / ivNitrates + Hydralazine in intoleranceto ACE-I (hypotension, renal insufficiency)44Treatment of Heart Failure.Nitrates: Use in Heart FailureThrough venodilation, nitrates reduce LVEDP, PAD, and PCWP, thereby improving pulmonary congestion and exercise tolerance. The reduction in end-diastolic pressure and volume decrease wall tension and oxygen consumption. Cardiac output and arterial pressure are not significantly changed, although a decrease in the LVEDP of 12 mmHg can decrease cardiac output. Nitrates are particularly useful in patients with signs of pulmonary congestion (PCWP > 18 mm Hg) and normal cardiac outputs, or in patients with orthopnea and PND. Recommended doses are well tolerated and rarely cause reflex tachycardia or hypotension. In patients with acute heart failure accompanied by pulmonary edema nitroglycerine can be given sublingually or i.v. I.V. administration allows for immediate onset of action, and rapid disappearance of effect within 10-30 minutes of stopping the infusion. Patients receiving I.V. nitroglycerin should be monitored. In patients with low cardiac output, nitrates can be used in conjunction with arterial vasodilators, dopamine, or dobutamine. In the treatment of chronic heart failure preparations with long half-lives are used. Topical nitroglycerine and other nitrates administered qHS are effective in patients with orthopnea and PND.Heart Transplant. IndicationsRefractory cardiogenic shockPeak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularizationRecurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalitiesContraindications: age, severe comorbidity45Heart Failure and Myocardial IschemiaCoronary HD is the cause of 2/3 of HFSegmental wall motion abnormalities are not specific if ischemiaAngina coronary angio and revascularizationNo angina Search for ischemia and viability in all ? Coronary angiography in all ?46Treatment of Heart Failure.Correction of aggravating factorsOften a lack of response to conventional therapy for heart failure is due to the presence of uncorrected aggravating or precipitating factors. It is important to always consider the possibility of such factors, particularly in cases of refractory failure. AF: atrial fibrillation.HEART FAILURE MODELSCONGESTIVE - Digoxin, DiurticsHEMODYNAMIC - VasodilatorsNEUROHUMORAL - ACE inhibitors, - Blockers, SpironolactoneIMMUNOLOGICAL - Cytokine inhibitors47Despite advances in treatment of systolic heart failure, our pending task is diastolic heart failure that appears isolated in 40% of patients. Symptomatic treatment includes administration of nitrates and adequate doses of diuretics. Studies suggest that beta blockers (BB) and calcium channel blockers (CCB) could be beneficial in some patient subgroups. We dont know about the effects of ACE inhibitors in these patients, although because of their antihypertensive, antiproliferative and antianginal properties could be expected to have beneficial effects. THANK YOU