2Low-Output Heart Failure Systolic Heart Failure (HFREF):Decreased Left ventricular ejection fractionDiastolic Heart Failure (HFPEF):Elevated Left and Right ventricular end-diastolic pressuresNormal LVEFHigh-Output Heart FailureSeen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism, beri-beri, carcinoid, anemiaOften have normal cardiac outputRight-Ventricular FailureSeen with pulmonary hypertension, large RV infarctions.
8Clinical Presentation of Heart Failure Due to excess fluid accumulation:Dyspnea (most sensitive symptom)EdemaHepatic congestionAscitesOrthopnea, Paroxysmal Nocturnal Dyspnea (PND)Due to reduction in cardiac ouput:Fatigue (especially with exertion)Weakness
9Cool, pale, cyanotic extremities S3 gallopLow sensitivity, but highly specificCool, pale, cyanotic extremitiesHave sinus tachycardia, diaphoresis and peripheral vasoconstrictionCrackles or decreased breath sounds at bases (effusions) on lung examElevated jugular venous pressureLower extremity edemaAscitesHepatomegalySplenomegalyDisplaced PMIApical impulse that is laterally displaced past the midclavicular line is usually indicative of left ventricular enlargement>
10Lab Analysis in Heart Failure CBCSince anemia can exacerbate heart failureSerum electrolytes and creatininebefore starting high dose diureticsFasting Blood glucoseTo evaluate for possible diabetes mellitusThyroid function testsSince thyrotoxicosis can result in A. Fib,and hypothyroidism can results in HF.Iron studiesTo screen for hereditary hemochromatosis as cause of heart failure.ANATo evaluate for possible lupusViral studiesIf viral mycocarditis suspected
11Laboratory Analysis (cont.) BNPWith chronic heart failure, atrial mycotes secrete increase amounts of atrial natriuretic peptide (ANP) and brain natriuretic pepetide (BNP) in response to high atrial and ventricular filling pressuresUsually is > 400 pg/mL in patients with dyspnea due to heart failure.
12Chest X-ray in Heart Failure CardiomegalyCephalization of the pulmonary vesselsKerley B-linesPleural effusions
16Cardiac Testing in Heart Failure Electrocardiogram:May show specific cause of heart failure:Ischemic heart diseaseDilated cardiomyopathy: first degree AV block, LBBB, Left anterior fascicular blockAmyloidosis: pseudo-infarction patternIdiopathic dilated cardiomyopathy: LVHEchocardiogram:Left ventricular ejection fractionStructural/valvular abnormalities
17Further Cardiac Testing in Heart Failure Coronary arteriographyShould be performed in patients presenting with heart failure who have angina or significant ischemiaReasonable in patients who have chest pain that may or may not be cardiac in origin, in whom cardiac anatomy is not known, and in patients with known or suspected coronary artery disease who do not have angina.Measure cardiac output, degree of left ventricular dysfunction, and left ventricular end-diastolic pressure.
19Classification of Heart Failure ACCF/AHA Stages of HFNYHA Functional ClassificationAAt high risk for HF but without structural heart disease or symptoms of HF.NoneBStructural heart disease but without signs or symptoms of HF.INo limitation of physical activity. Ordinary physical activity does not cause symptoms of HF.CStructural heart disease with prior or current symptoms of HF.IISlight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF.IIIMarked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF.IVUnable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest.DRefractory HF requiring specialized interventions.
20Aggravating Factors Medications New heart disease Myocardial ischemia PregnancyArrhythmias (AF)InfectionsThromboembolismHyper/hypothyroidismEndocarditisObesityHypertensionPhysical activityDietary excessTreatment 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.
21Heart Failure and Myocardial Ischemia Coronary HD is the cause of 2/3 of HFSegmental wall motion abnormalities are not specific if ischemiaAngina coronary angio and revascularizationNo anginaSearch for ischemia and viability in all ?Coronary angiography in all ?Treatment 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.
22ACE-i. Mechanism of Action VASOCONSTRICTIONVASODILATATIONALDOSTERONEPROSTAGLANDINSVASOPRESSINKininogentPASYMPATHETICKallikreinAngiotensinogenRENINBRADYKININTreatment 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.Angiotensin IA.C.E.InhibitorKininase IIANGIOTENSIN IIInactive Fragments
23ACE-I. Clinical Effects Improve symptomsReduce remodelling / progressionReduce hospitalizationImprove survivalTreatment 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.
24Mortality Reduction with ACE-i Study ACE-i Clinical SetingCONSENSUS Enalapril CHFSOLVD treatment Enalapril CHFAIRE Ramipril CHFVheft-II Enalapril CHFTRACE Trandolapril CHF / LVDSAVE Captopril LVDSMILE Zofenopril High riskHOPE Ramipril High risk
25ACE-i Placebo Probabiility of Death Enalapril CONSENSUS Months 0.8 0.7 0.6Probabiility ofDeathp< 0.0010.50.4p< 0.0020.3EnalaprilTreatment of Heart Failure.Angiotensin Converting-Enzyme Inhibitors (ACEI): SurvivalCONSENSUS. Prolonged administration of ACE-inhibitors reduces mortality in symptomatic heart failure. The first study to demonstrate this effect was CONSENSUS I. This graph shows the cumulative mortality curves of the treatment and placebo group in this randomized, double-blind trial. The study analyzed the effect of enalapril on prognosis of 253 patients with class IV heart failure, who also received digitalis, diuretics, and conventional vasodilators. At the end of 6 months of treatment, there was a clear-cut improvement in functional class, a reduction in the need for medications, and a 40% reduction in mortality (p<0.002). After 12 months the mortality reduction was 31% (p<0.001). Nonetheless, there were no differences in the incidence of sudden death between the two groups, or in the sub-group that received other conventional vasodilators. Another characteristic of this study was variability of the dose that was used for each patient (adjusted for tolerance and symptoms): mg/day. This aspect shows the importance of individualized treatment for heart failure patients.The CONSENSUS Trial Study Group. N Engl J Med 1987;316:14220.127.116.113456789101112CONSENSUSN Engl J Med 1987;316:1429Months
26ACE-i Mortality, % Years SAVE 30 Placebo 20 Captopril 10 1 2 3 4 Asymptomaticventriculardysfunction post MIPlacebon=111620Mortality,%Captopriln=1115Treatment of Heart FailureAngiotensin Converting-Enzyme Inhibitors (ACEI): SurvivalSAVE (Survival and Ventricular Enlargement). Mortality curves in the SAVE study in patients with varying degrees of post-infarct ventricular dysfunction. In this study, 2231 patients with EF < 40% were randomized to receive captopril or placebo between 3 to 16 days after experiencing a transmural infarct. After 42 months, the captopril group had a significant reduction in overall mortality (-19%), number of reinfarctions (-25%), hospitalizations (-22%), and in the number of patients who developed clinical congestive heart failure. The mortality reduction appeared after 1 year of treatment.Pfeffer MA et al. Survival and Ventricular Enlargement (SAVE) Study. NEngl J Med 1992;327:669.10n = 2231days post AMIEF < 40mg / day² -19%p=0.019SAVEN Engl J Med 1992;327:6691234Years
27ACE-i. Indications Symptomatic heart failure Asymptomatic ventricular dysfunction- LVEF < %Selected high risk subgroupsTreatment 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%.AHA / ACC HF guidelines 2001ESC HF guidelines 2001
28ACE-i. Practical Use Start with very low dose Increase dose if well toleratedRenal function & serum K+ after 1-2 wAvoid fluid retention / hypovolemia (diuretic use)Dose NOT determined by symptoms
29ACE-i. Dose (mg) Initial Maximum Captopril 6.25 / 8h 50 / 8h Enalapril 2.5 / 12 h 10 to 20 / 12hFosinopril 5 to 10 / day 40 / dayLisinopril 2.5 to 5.0 / day 20 to 40 / dayQuinapril 10 / 12 h 40 / 12 hRamipril to 2.5 / day 10 / dayAHA / ACC HF guidelines 2001
30Hypotension (1st dose effect) Worsening renal function Hyperkalemia ACE-I. Adverse EffectsHypotension (1st dose effect)Worsening renal functionHyperkalemiaCoughAngioedemaRash, ageusia, neutropenia, …Treatment 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).
31ACE-I. Contraindications Intolerance (angioedema, anuric renal fail.)Bilateral renal artery stenosisPregnancyRenal insufficiency (creatinine > 3 mg/dl)Hyperkalemia (> 5,5 mmol/l)Severe hypotensionTreatment 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.
32ß-Adrenergic Blockers Mechanism of action Density of ß1 receptorsInhibit cardiotoxicity of catecholaminesNeurohormonal activationHRAntiischemicAntihypertensiveAntiarrhythmicAntioxidant, AntiproliferativeTreatment of congestive heart failure.Possible benefits of beta adrenergic blockersThe use of ß-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.
37- Spironolactone Aldosterone Inhibitors ALDOSTERONE Edema Fibrosis Competitive antagonist of thealdosterone receptor(myocardium, arterial walls, kidney)Retention Na+Retention H2OExcretion K+Excretion Mg2+CollagendepositionFibrosis- myocardium- vesselsEdemaTreatment of congestive heart failure.Aldosterone inhibitors: Mechanism of actionAldosterone 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.Arrhythmias
38Spironolactone Survival RALES Aldactone N = 1663 NYHA III-IV 1.00.90.80.70.60.5Annual MortalityAldactone 18%; Placebo 23%SurvivalAldactoneN = 1663NYHA III-IVMean follow-up 2 yMortality curves in the RALES study. (probably already shown by previous speaker). I will coment on the progressive increase in benefit and will made a comparation with the CIBIS-II results.p <RALESNEJM 1999;341:709monthsPlacebo61218243036
39Spironolactone. Indications Recent or current symptoms despite ACE-i, diuretics, dig. and b-blockersAHA / ACC HF guidelines 2001Recommended in advanced heart failure (III-IV), in addition to ACE-i and diureticsHypokalemiaESC HF guidelines 2001
40Spironolactone. Practical use Do not use if hyperkalemia, renal insuf.Monitor serum K+ at “frequent intervals”Start 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 / dayNew studies in progress
41Angiotensin I ANGIOTENSIN II Angiotensin II Receptor Blockers (ARB)RENINAngiotensinogenAngiotensin I ANGIOTENSIN IIACEOther pathwaysAT1ReceptorBlockersTreatment of congestive heart failure.Angiotensin II inhibitorsAngiotensin 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.RECEPTORSAT1AT2VasoconstrictionProliferativeActionVasodilatationAntiproliferativeAction
42Angiotensin II Receptor Blockers (ARB) Candesartan, Eprosartan, IrbesartanLosartan, Telmisartan, ValsartanNot indicated with beta blockersIndicated in patients intolerant to ACE-ITreatment of congestive heart failure.Angiotensin II inhibitorsDrugs which create a selective and competitive block of the AT1 receptors include: losartan, valsartan, irbersartan and candersartan.AHA / ACC HF guidelines 2001ESC HF guidelines 2001
43Positive Inotropes Digitalis Sympathomimetics Catecholamines B-adrenergic agonistsPhosphodiesterase inhibitorsAmrinone, Milrinone, EnoximoneCalcium sensitizersLevosimendan, PimobendanTreatment of heart failure.Positive inotropic agentsThe use of inotropic agents in heart failure is intended to increase contractility and cardiac output to meet the metabolic needs of the body. Theoretically, their use should be greatest in heart failure associated with a decrease in systolic function and marked cardiomegaly, depression of ejection fraction and elevated left ventricular filling pressure. In addition to the cardiac glycosides, other positive inotropic agents include: a) the sympathomimetics, represented by the ß1 agonists (which stimulate cardiac contractility) and ß2-adrenergics (vasodilators). Both groups increase the intracellular concentration of cAMP by stimulating the activity of adenylate cyclase which converts ATP to cAMP; b) Phosphodiesterase inhibitors, which inhibit the enzyme that breaks down cAMP, increase cardiac contractility and have arteriovenous vasodilatory effect; c) other ionotropic drugs including glucagon and Na+ channels agonists.
44Positive Inotropic Therapy May increase mortalityException: Digoxin, LevosimendanUse only in refractory CHFNOT for use as chronic therapyTreatment of heart failure.Inotropes: General problemsPositive inotropic drugs which increase cellular levels of cAMP have important proarrhythmic effects and seem to accelerate the progression of heart failure. Their hemodynamic effects decreased with prolonged treatment which suggests that they should not be used for chronic treatment. Safety and efficacy increases when they are used in low doses, with which the increase in contractility is slight. This points out that their beneficial effects probably do not depend on their positive inotropic action. The reduction in neurohumoral activation produced by digoxin and ibopamine, the antiarrhythmic action of Vesnarinone or the vasodilatory effects of dopamine, dobutamine or PDE III inhibitors may be more important than the increase in contractility that until recently was though to be their utility in the treatment of heart failure. With the exception of digoxin, chronic administration of these drugs increases mortality, so their use, in low doses, should be restricted to patients with refractory heart failure, with persistent symptoms despite treatment with combinations of other drugs. As it is precisely the sickest patients who manifest the increase in mortality, treatment with inotropic drugs is not likely to prolong the survival of these patients.
46Digitalis. Clinical Effects Improve symptomsModest reduction in hospitalizationDoes not improve survivalTreatment 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.
47Digitalis. Indications • When no adequate response toACE-i + diuretics + beta-blockersAHA / ACC Guidelines 2001• In combination with ACE-i + diureticsif persisting symptomsESC Guidelines 2001• AF, to slow AV conductionDose to mg / day
48Digitalis Mortality % 50 40 30 20 10 Placebo Digoxin DIG 12 24 36 48 Mortality%Placebon=3403p = 0.8N=6800NYHA II-IIITreatment of heart failure.Digoxin: Effect on survivalThe results obtained from 3 controlled studies which included patients at low risk (The German and Austrian Xamoterol Study Group, 1988; The Captopril-Digoxin Multicenter Research Group, 1988; DiBianco et al., 1989) indicate that the mortality was similar in the group of patients with placebo. The results of the Digitalis Investigator Group-DIG study, which included 7788 patients with heart failure in sinus rhythm, functional class II-III and LVEF < 45%. The patients were treated with digoxin or placebo, in addition to conventional therapy over a mean of 37 months ( months). No differences in mortality were observed between the two treatment groups.Am Coll Cardiol 1996Digoxinn=3397DIGN Engl J Med 1997;336:52512243648Months
50Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weightMonitor serum K+ at “frequent intervals”Reduce dose when fluid retention is controlledTeach the patient when, how to change doseCombine to overcome “resistance”Do not use alone
51Thiazides, Loop Diuretics. Adverse Effects • K+, Mg+ ( %) (sudden death ???)• Na+• Stimulation of neurohormonal activity• Hyperuricemia ( %)• Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. MetabolicSharpe 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;635
52Diuretic Resistance Neurohormonal activation Rebound Na+ uptake after volume lossHypertrophy of distal nephronReduced tubular secretion (renal failure, NSAIDs)Decreased renal perfusion (low output)Altered absortion of diureticNoncompliance with drugsBrater NEJM 1998;339:387Kramer et al. Am J Med 1999;106:90
53Managing Resistance to Diuretics • Restrict Na+/H2O intake (Monitor Natremia)• Increase dose (individual dose, frequency, i.v.)• Combine: furosemide + thiazide / spiro / metolazone• Dopamine (increase cardiac output)• Reduce dose of ACE-i• UltrafiltrationMotwani et al Circulation 1992;86:439
54Drugs to Avoid (may increase symptoms, mortality) Inotropes, long term / intermittentAntiarrhythmics (except amiodarone)Calcium antagonists (except amlodipine)Non-steroidal antiinflammatory drugs (NSAIDS)Tricyclic antidepressantsCorticosteroidsLithiumESC HF guidelines 2001
56Cardiac Resynchronization Therapy Cardiac Resynchronization Therapy* in Patients With Severe Systolic Heart FailureFor patients who have left ventricular ejection fraction (LVEF) less than or equal to 35%, a QRS duration greater than or equal to 0.12 seconds, and sinus rhythm, cardiac resynchronization therapy (CRT) with or without an ICD is indicated for the treatment of New York Heart Association (NYHA) functional Class III or ambulatory Class IV heart failure symptoms on optimal recommended medical therapy
58Heart Transplant. Indications Refractory cardiogenic shockDocumented dependence on IV inotropic support to maintain adequate organ perfusionPeak VO2 < 10 ml / kg / minSevere symptoms of ischemia not amenable to revascularizationRecurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalitiesContraindications: age, severe comorbidity
59Ventricular Arrhythmias / Sudden Death Antiarrhythmics ineffective (may increase mortality)Amiodarone do not improve survival-blockers reduce all cause mortality and SDControl ischemiaControl electrolyte disturbancesICD (Implantable Cardiac Defibrillator)In secondary prevention of SDIn sustained, hemodynamic destabilizing VTOngoing research will establish new indicationsTreatment 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.
60Device Therapy for Stage C HFrEF (cont.) RecommendationsCORLOEICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤35%, and NYHA class II or III symptoms on chronic GDMT, who are expected to live ≥1 year*IACRT is indicated for patients who have LVEF ≤35%, sinus rhythm, LBBB with a QRS ≥150 msA (NYHA class III/IV)B (NYHA class II)ICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤30%, and NYHA class I symptoms while receiving GDMT, who are expected to live ≥1 year*BCRT can be useful for patients who have LVEF ≤35%, sinus rhythm, a non-LBBB pattern with a QRS ≥150 ms, and NYHA class III/ambulatory class IV symptoms on GDMT.IIaCRT can be useful for patients who have LVEF ≤35%, sinus rhythm, LBBB with a QRS 120 to 149 ms, and NYHA class II, III or ambulatory IV symptoms on GDMTCRT can be useful in patients with AF and LVEF ≤35% on GDMT if a) the patient requires ventricular pacing or otherwise meets CRT criteria and b) AV nodal ablation or rate control allows near 100% ventricular pacing with CRTslide 3760
61Diastolic Heart Failure Incorrect diagnosis of HFInaccurate measurement of LVEFPrimary valvular diseaseRestrictive (infiltrative) cardiomyopathies (Amyloidosis…)Pericardial constrictionEpisodic or reversible LV systolic dysfunctionSevere hypertension, ischemiaHigh output states: Anemia, thyrotoxicosis, etcChronic pulmonary disease with right HFPulmonary hypertensionAtrial myxomaLV HypertrophyDiastolic dysfunction of uncertain origin
62Treatment of HFpEF Recommendations COR LOE Systolic and diastolic blood pressure should be controlled according to published clinical practice guidelinesIBDiuretics should be used for relief of symptoms due to volume overloadCCoronary revascularization for patients with CAD in whom angina or demonstrable myocardial ischemia is present despite GDMTIIaManagement of AF according to published clinical practice guidelines for HFpEF to improve symptomatic HFUse of beta-blocking agents, ACE inhibitors, and ARBs for hypertension in HFpEFARBs might be considered to decrease hospitalizations in HFpEFIIbNutritional supplementation is not recommended in HFpEFIII: No Benefit