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Management of chest pain and heart failure. Cardiac rehabilitation and secondary prevention WT Bong Dept of Family Medicine, HUKM Case scenario 1 • 60 yo gentleman, a known case of DM for the past 2 years complains of chest pain for the past 2-3 months when he walks more than 10 minutes. The chest pain radiates to left arm, lasts 5 min, relieved by rest. Currently during his visit to the primary care clinic, he has no chest pain. He is a smoker for the past 40 years. He is on metformin 500mh bd only. Clinically, BP 120/60mmHg and cardiovascular examination was unremarkable. Patient comes in with chest pain.. • ?cardiovascular – Cardiac. • MV prolapse.pericarditis • ischemic – Non cardiac. Aortic dissection • • • • ?gastrointestinal. GERD ?Musculoskeletal.fibromyalgia. ?pulmonary ?psychogenic Patient comes in with chest pain.. • ?cardiovascular – Cardiac. • MV prolapse.pericarditis • ischemic – Non cardiac. Aortic dissection • • • • ?gastrointestinal. GERD ?Musculoskeletal.fibromyalgia. ?pulmonary ?psychogenic We start with stable angina.. • By definition. Clinical syndrome characterised by – discomfort in chest, jaw, shoulder, back or arm – Typically aggravated by exertion or emotional stress – Reduced by rest or GTN • Most common cause for stable angina is atherosclerotic coronary artery disease (CAD) • Other causes could be – Hypertrophic cardiomyopathy – Aortic stenosis – Coronary vasospasm etc Atherosclerosis process in coronary Stable angina is classified into 4 classes based on Canadian Cardiovascular Society Classification (CCS 0-IV) CLASS SEVERITY OF EXERTIONL STRESS INDUCING ANGINA LIMITATION OF ORDINARY ACTIVITY I STRENUOUS, RAPID OR PROLONGED EXERTION AT WORK OR RECREATION NONE II WALKING OR CLIMBING STAIRS RAPIDLY, WALKING UPHILL, CLIMBING STAIRS AFTER MEAL SLIGHT III WALKING 1-2 BLOCKS ON THE LEVEL AND CLIMBING ONE FLIGHT OF STAIRS AT NORMAL PACE MARKED IV INABILITY TO CARRY OUT ANY PHYSICAL ACTIVITY WITHOUR DISCOMFORT OR SYMPTOMS PRESENT AT REST DISCOMFORT IN ALL ACTIVITY PERFORMED • However, it might become unstable, which is unstable angina, with possible progression to NSTEMI and STEMI too Diagnosis of stable angina can be established by • Clinical assessment – Look for complication of CAD.murmur(MR).septal defect.sign of cardiomegaly.CHF – Other site of atherosclerosis.carotid bruit.peripheral vascular disease.aortic aneurysm – Risk factor for atherosclerosis.hpt.metabolic syn – Other cause of angina.HOCM.aortic stenosis • Lab test • Specific cardiac investigation • Lab test to establish CVS risk factor – FLP. FBS. homocysteine level – Determine prognosis, creatinine – CXR only if suspect CHF if want to see calcification, cardiomegaly/atrial enlargement, valvular disease, pulmonary congestion (help establish prognosis) • Specific cardiac investigation • Specific cardiac investigation, non invasive – ECG. See previous ischemia, LVH, BBB, arrhythmia or conduction defect – Stress test. More sensitive and specific than resting ECG – Echo.when there is abnormal auscultation suggest valvular, if HCM or prev MI changes on ECG, SSx CHF , to study diastolic function Risk-stratify our patient • For the purpose of prognosis + treatment (revascularize in high risk patient) Clinical history – important predictor of adverse outcome in established CAD DM HPT Metabolic syndrome Current smoker Increasing age Prior MI SSx of CHF Recent onset or progressive angina dyslipidaemia Responsiveness of angina to therapy Risk stratify .. Higher risk if ECG shows Evidence of prior MI LBBB LVH AF Second of third degree AV block Other aspects to be considered in riskstratifying • Stress test • Ventricular function • COROS LVEF < 35 % 12- year survival rate (p<0.0001) 21 % 35-49 % 54 % > 50 % 73 % Treatment goal • Prevent MI & death • Improve SSx of angina & increase QoL Non pharmacological approach Life style • Smoking cessation – 36 % risk reduction mortality – 32 % risk reduction non fatal MI – Nicotine replacement is safe and cost effective even for CAD patient (take into account risk of depression and suicidal thought) diet • Variety of fruits and vegetable.legumes.nuts. Soy products.low fat dairy.whole grain • Replace saturated & transfat (red meat.whole milk . Pastries) with polysaturated fat (oily fish,walnut,sesame. Pumpkin seed.vegetable oil) • Soluble fibre.oat.peas.bean Alcohol restriction. Moderate/beneficial. Insufficient evidence Physical activity. 30min 3-4x/week Target BP <130/80 DM Generally target HbA1c < 6.5 %. Individualize as Keep waist circumference < 85 cm for men < 80 cm for women Correct anaemia Correct hyperthyroid state HDL > 1.0 male, 1.2 female ( secondary target) TG < 1.7 (secondary target) hypoglycemia worsen angina & increase mortality LDL < 1.8 ( primary target) education Self management During acute anginal attack -Restrain activity -GTN S/L or spray -Sit . Hypotension. Headache after GTN Can also take GTN as preventive measure if patient know he is going to have attack while carrying out some activity If SSx persist more than 10min at rest or not improved after 3 tablet of GTN, advice to go to hospital Antithrombotic Antithrombotic ASA 75-150mg od. Lower MI, cardiac death Clopidogrel 75mg -more effective than ASA in peripheral vascular disease or stroke Take into account GI side effect *double antiplatelet not warranted in angina Ticlopidine – proven efficacy in stroke and post-PCI, no evidence in angina Lipid lowering ACEi Statin reduce mortality & CV event by 20 – 30 % For secondary prevention in post MI + reduced EF < 40 % Can add ezetimide if target not reached with statin Recommended for all patients with CAD esp with concomitant LV dysfunction/DM ARB Beta blocker \as secondary prevention in CAD with Hpt/ CHF / post MI + LV dysfunction / DM if not tolerable to ACEi First line treatment in angina - 30 % reduction risk of CV death / MI (beta blocker in post MI trials) -Beta1 blockade by Metoprolol/bisoprolol reduce cardiac event in CHF -Non selective beta blockade by carvedilol reduce death & CV hospitalisation in CHF Ivabradine Calcium Channel Blocker HR reducing, acting on SA node -non dihydropyridine – diltiazem/verapamil, Symptomatic treatment in patient with N`SR, as alternative to beta blocker esp with contraindication for beta blocker -dihydropyridine (long acting) –amlodipine No significant interaction with other cardiac use in patient reduce coronary intervention but no reduction in treatment endpoints (ie death , MI) drugs Nitrates Trimetazidine (long acting – isordil,imdur) (Vasteral MR) Symptomatic improvement of angina No prognostic benefit symptomatic relief of angina Safe and effective in patient with ED Dipyridamole Anticoagulant Not indicated unless has AF (Persanthine) not recommended, poor antithrombotic efficacy in angina revascularization • PCI or CABG – In high risk group it is firstline treatment • Significant LMS ( > 50% stenosis) • Significant proximal mutivessel involvement • Multivessel disease with impaired LV function with proven viable myocardium – Or if failed medical treatment to control angina SSx – In asymptomatic patient, consider if there is extensive inducible ischaemia (stress test) What if it is aMI ? Chest pain ECG ,cardiac biomarker STEMI Concomitant initial management Sublingual GTN, continuous ECG monitoring, oxygen, ASA, clopidogrel, analgesia Assessment for reperfusion < 3hrs 3-12hrs > 12 hrs Onset of symptoms < 3 hrs 3-12 hrs > 12 hrs Preferred options Primary PCI (if door to balloon time < Medical therapy +/anti thrombotics Primary PCI (preferred in high risk patient or contraindicated for thrombolytic) or 90min) fibrinolytic Second options fibrinolytics Primary PCI ( if clinically indicated) Concomitant therapy Anti thrombotics Beta blockers ACEi / ARB Statins Nitrates CCB Secondary prevention • Basically similar to angina which include Smoking cessation diet Regular exercise BP control Glycemic control Antiplatelet agent *consider dual antiplatelet 1mth-1yr depend on stent used Beta blocker ACEi and ARB Lipid lowering • Oral Anticoagulant (warfarin) – If AF – LV thrombus for 3-6mths Secondary prevention • Hormone replacement therapy is not beneficial for secondary prevention • Postmenopausal women who were taking HRT at the time of STEMI should discontinue it • Vitamin E and antioxidants have no clinical benefit • Garlic, lecithin, vitamin A and C are not beneficial Heart failure Heart failure • Is a complex clinical syndrome results from structural or functional impairment of ventricular filling or ejection of blood • Cardinal manifestation are dyspnea, fatigue, which may limit effort tolerance, and fluid retention, which may lead to pulmonary or splanchnic congestion or peripheral edema. Definition of Heart Failure Classification I. Heart Failure with Reduced Ejection Fraction (HFrEF) Ejection Fraction ≤40% Description Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients that efficacious therapies have been demonstrated to date. ≥50% Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified. a. HFpEF, Borderline 41% to 49% These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF. b. HFpEF, Improved >40% It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients. II. Heart Failure with Preserved Ejection Fraction (HFpEF) Stages, Phenotypes and Treatment of HF At Risk for Heart Failure Heart Failure STAGE A STAGE B STAGE C At high risk for HF but without structural heart disease or symptoms of HF Structural heart disease but without signs or symptoms of HF Structural heart disease with prior or current symptoms of HF e.g., Patients with: · HTN · Atherosclerotic disease · DM · Obesity · Metabolic syndrome or Patients · Using cardiotoxins · With family history of cardiomyopathy Structural heart disease e.g., Patients with: · Previous MI · LV remodeling including LVH and low EF · Asymptomatic valvular disease Development of symptoms of HF e.g., Patients with: · Known structural heart disease and · HF signs and symptoms HFpEF THERAPY Goals · Heart healthy lifestyle · Prevent vascular, coronary disease · Prevent LV structural abnormalities Drugs · ACEI or ARB in appropriate patients for vascular disease or DM · Statins as appropriate THERAPY Goals · Prevent HF symptoms · Prevent further cardiac remodeling Drugs · ACEI or ARB as appropriate · Beta blockers as appropriate In selected patients · ICD · Revascularization or valvular surgery as appropriate STAGE D Refractory HF THERAPY Goals · Control symptoms · Improve HRQOL · Prevent hospitalization · Prevent mortality Strategies · Identification of comorbidities Treatment · Diuresis to relieve symptoms of congestion · Follow guideline driven indications for comorbidities, e.g., HTN, AF, CAD, DM · Revascularization or valvular surgery as appropriate Refractory symptoms of HF at rest, despite GDMT e.g., Patients with: · Marked HF symptoms at rest · Recurrent hospitalizations despite GDMT HFrEF THERAPY Goals · Control symptoms · Patient education · Prevent hospitalization · Prevent mortality Drugs for routine use · Diuretics for fluid retention · ACEI or ARB · Beta blockers · Aldosterone antagonists Drugs for use in selected patients · Hydralazine/isosorbide dinitrate · ACEI and ARB · Digoxin In selected patients · CRT · ICD · Revascularization or valvular surgery as appropriate THERAPY Goals · Control symptoms · Improve HRQOL · Reduce hospital readmissions · Establish patient’s endof-life goals Options · Advanced care measures · Heart transplant · Chronic inotropes · Temporary or permanent MCS · Experimental surgery or drugs · Palliative care and hospice · ICD deactivation Classification of Heart Failure A B C ACCF/AHA Stages of HF At high risk for HF but without structural heart disease or symptoms of HF. Structural heart disease but without signs or symptoms of HF. Structural heart disease with prior or current symptoms of HF. NYHA Functional Classification None I I II III IV D Refractory HF requiring specialized interventions. No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. Physical examination • • • • • • • • BMI and evidence of weight loss Bp, supine and upright( orthostatic changes – volume depletion) Pulse – strength and regularity JVP Extra heart sound, murmur, apex beat displacement, RV heave Pulmonary status Hepatomegaly Peripheral edema Lab investigation • • • • • • • Class I 1.Initial laboratory evaluation of patients presenting with HF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroidstimulating hormone. (Level of Evidence: C) 2.Serial monitoring, when indicated, should include serum electrolytes and renal function. (Level of Evidence: C) 3.A 12-lead ECG should be performed initially on all patients presenting with HF. (Level of Evidence: C) Class Iia 1.Screening for hemochromatosis or HIV is reasonable in selected patients who present with HF (Level of Evidence: C) 2.Diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma are reasonable in patients presenting with HF in whom there is a clinical suspicion of these diseases. (Level of Evidence: C) Recommendations for Biomarkers in HF Biomarker, Application Setting COR LOE Diagnosis or exclusion of HF Ambulatory, Acute I A Prognosis of HF Ambulatory, Acute I A Ambulatory IIa B Acute IIb C Acute, Ambulatory I A IIb B IIb A Natriuretic peptides Achieve GDMT Guidance of acutely decompensated HF therapy Biomarkers of myocardial injury Additive risk stratification Biomarkers of myocardial fibrosis Ambulatory Additive risk stratification Acute Recommendations for Noninvasive Imaging Recommendation Patients with suspected, acute, or new-onset HF should undergo a chest xray A 2-dimensional echocardiogram with Doppler should be performed for initial evaluation of HF Repeat measurement of EF is useful in patients with HF who have had a significant change in clinical status or received treatment that might affect cardiac function, or for consideration of device therapy Noninvasive imaging to detect myocardial ischemia and viability is reasonable in HF and CAD Viability assessment is reasonable before revascularization in HF patients with CAD Radionuclide ventriculography or MRI can be useful to assess LVEF and volume MRI is reasonable when assessing myocardial infiltration or scar Routine repeat measurement of LV function assessment should not be performed COR LOE I C I C I C IIa C IIa B IIa C IIa B III: No Benefit B ACC AHA heart failure 2013 • Treament based on stages of heart failure ACCF/AHA Stages of HF NYHA Functional Classification A At high risk for HF but without structural heart disease or symptoms of HF none B Structural heart disease but without signs or symptoms of HF I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. C Structural heart disease with prior or current symptoms of HF I No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. III Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. IV Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. D Refractory HF requiring specialized interventions ACC AHA heart failure 2013 • Stage A: Recommendations • Class I • 1.Hypertension and lipid disorders should be controlled in accordance with contemporary guidelines to lower the risk of HF(Level of Evidence: A) • 2.Other conditions that may lead to or contribute to HF, such as obesity, diabetes mellitus, tobacco use, and known cardiotoxic agents, should be controlled or avoided. (Level of Evidence: C) HFSA 2010 Practice Guideline (3.1) Heart Failure Prevention A careful and thorough clinical assessment, with appropriate investigation for known or potential risk factors, is recommended in an effort to prevent development of LV remodeling, cardiac dysfunction, and HF. Strength of Evidence = A Adapted from: HFSA 2010 Practice Guideline (3.2) HF Risk Factor Treatment Goals Risk Factor Goal Hypertension Generally < 130/80 Diabetes See ADA guidelines1 Hyperlipidemia See NCEP guidelines2 Inactivity 20-30 min. aerobic 3-5 x wk. Obesity Weight reduction < 30 BMI Alcohol Men ≤ 2 drinks/day, women ≤ 1 Smoking Cessation Dietary Sodium Maximum 2-3 g/day 1Diabetes 2JAMA Adapted from: Care 2006; 29: S4-S42 2001; 285:2486-97 Treating Hypertension to Prevent HF Aggressive blood pressure control: Decreases risk of new HF by ~ 50% 56% in T2DM Lancet 1991;338:1281-5 (STOP-Hypertension JAMA 1997;278:212-6 (SHEP) UKPDS Group. UKPDS 38. BMJ 1998;317:703-713 Aggressive BP control in patients with prior MI: Decreases risk of new HF by ~ 80% HFSA 2010 Practice Guideline (3.3-3.4) Prevention—ACEI and Beta Blockers ACE inhibitors are recommended for prevention of HF in patients at high risk for this syndrome, including those with: – Coronary artery disease – Peripheral vascular disease – Stroke – Diabetes and another major risk factor Strength of Evidence = A ACE inhibitors and beta blockers are recommended for all patients with prior MI. Strength of Evidence = A HFSA 2010 Practice Guideline (4.8, 4.10) Heart Failure Patient Evaluation Recommended evaluation for patients with a diagnosis of HF: – Assess clinical severity and functional limitation by history, physical examination, and determination of functional class* – – – – – – – Assess cardiac structure and function Determine the etiology of HF Evaluate for coronary disease and myocardial ischemia Evaluate the risk of life threatening arrhythmia Identify any exacerbating factors for HF Identify co-morbidities which influence therapy Identify barriers to adherence and compliance Strength of Evidence = C *Metrics to consider include the 6-minute walk test and NYHA functional class Adapted from: Recommendations for Treatment of Stage B HF Recommendations In patients with a history of MI and reduced EF, ACE inhibitors or ARBs should be used to prevent HF In patients with MI and reduced EF, evidence-based beta blockers should be used to prevent HF In patients with MI, statins should be used to prevent HF Blood pressure should be controlled to prevent symptomatic HF ACE inhibitors should be used in all patients with a reduced EF to prevent HF Beta blockers should be used in all patients with a reduced EF to prevent HF An ICD is reasonable in patients with asymptomatic ischemic cardiomyopathy who are at least 40 d post-MI, have an LVEF ≤30%, and on GDMT Nondihydropyridine calcium channel blockers may be harmful in patients with low LVEF COR LOE I A I B I A I A I A I C IIa B III: Harm C Treatment of Stages A to D Stage C Treatment of Stages A to D Nonpharmacological Interventions I IIa Stage C: Nonpharmacological Interventions IIb III Patients with HF should receive specific education to facilitate HF self-care. I IIa IIb III Exercise training (or regular physical activity) is recommended as safe and effective for patients with HF who are able to participate to improve functional status. I IIa IIb III Sodium restriction is reasonable for patients with symptomatic HF to reduce congestive symptoms. Treatment of Stages A to D Pharmacological Treatment for Stage C HFrEF Pharmacologic Treatment for Stage C HFrEF HFrEF Stage C NYHA Class I – IV Treatment: Class I, LOE A ACEI or ARB AND Beta Blocker For all volume overload, NYHA class II-IV patients For persistently symptomatic African Americans, NYHA class III-IV For NYHA class II-IV patients. Provided estimated creatinine >30 mL/min and K+ <5.0 mEq/dL Add Add Add Class I, LOE C Loop Diuretics Class I, LOE A Hydral-Nitrates Class I, LOE A Aldosterone Antagonist Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III Diuretics are recommended in patients with HFrEF who have evidence of fluid retention, unless contraindicated, to improve symptoms. I IIa IIb III ACE inhibitors are recommended in patients with HFrEF and current or prior symptoms, unless contraindicated, to reduce morbidity and mortality. I IIa IIb III ARBs are recommended in patients with HFrEF with current or prior symptoms who are ACE inhibitor-intolerant, unless contraindicated, to reduce morbidity and mortality. Drugs Commonly Used for HFrEF (Stage C HF) Drug ACE Inhibitors Captopril Enalapril Fosinopril Lisinopril Perindopril Quinapril Ramipril Trandolapril ARBs Candesartan Losartan Valsartan Aldosterone Antagonists Spironolactone Eplerenone Initial Daily Dose(s) Maximum Doses(s) Mean Doses Achieved in Clinical Trials 6.25 mg 3 times 2.5 mg twice 5 to 10 mg once 2.5 to 5 mg once 2 mg once 5 mg twice 1.25 to 2.5 mg once 1 mg once 50 mg 3 times 10 to 20 mg twice 40 mg once 20 to 40 mg once 8 to 16 mg once 20 mg twice 10 mg once 4 mg once 122.7 mg/d (421) 16.6 mg/d (412) --------32.5 to 35.0 mg/d (444) --------------------------------- 4 to 8 mg once 25 to 50 mg once 20 to 40 mg twice 32 mg once 50 to 150 mg once 160 mg twice 24 mg/d (419) 129 mg/d (420) 254 mg/d (109) 12.5 to 25 mg once 25 mg once 25 mg once or twice 50 mg once 26 mg/d (424) 42.6 mg/d (445) Drugs Commonly Used for HFrEF (Stage C HF) (cont.) Drug Initial Daily Dose(s) Beta Blockers Bisoprolol 1.25 mg once Carvedilol 3.125 mg twice Carvedilol CR 10 mg once Metoprolol succinate extended release 12.5 to 25 mg once (metoprolol CR/XL) Hydralazine & Isosorbide Dinitrate 37.5 mg hydralazine/ Fixed dose combination 20 mg isosorbide (423) dinitrate 3 times daily Hydralazine and Hydralazine: 25 to 50 isosorbide dinitrate (448) mg, 3 or 4 times daily and isorsorbide dinitrate: 20 to 30 mg 3 or 4 times daily Maximum Doses(s) Mean Doses Achieved in Clinical Trials 10 mg once 50 mg twice 80 mg once 8.6 mg/d (118) 37 mg/d (446) --------- 200 mg once 159 mg/d (447) 75 mg hydralazine/ 40 mg isosorbide dinitrate 3 times daily Hydralazine: 300 mg daily in divided doses and isosorbide dinitrate 120 mg daily in divided doses ~175 mg hydralazine/90 mg isosorbide dinitrate daily --------- Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III ARBs are reasonable to reduce morbidity and mortality as alternatives to ACE inhibitors as first-line therapy for patients with HFrEF, especially for patients already taking ARBs for other indications, unless contraindicated. I IIa IIb III Addition of an ARB may be considered in persistently symptomatic patients with HFrEF who are already being treated with an ACE inhibitor and a beta blocker in whom an aldosterone antagonist is not indicated or tolerated. Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III Routine combined use of an ACE inhibitor, ARB, and aldosterone antagonist is potentially harmful for patients with HFrEF. Harm I IIa IIb III Use of 1 of the 3 beta blockers proven to reduce mortality (i.e., bisoprolol, carvedilol, and sustained-release metoprolol succinate) is recommended for all patients with current or prior symptoms of HFrEF, unless contraindicated, to reduce morbidity and mortality. Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III Aldosterone receptor antagonists [or mineralocorticoid receptor antagonists (MRA)] are recommended in patients with NYHA class II-IV and who have LVEF of 35% or less, unless contraindicated, to reduce morbidity and mortality. Patients with NYHA class II should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists. Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III Aldosterone receptor antagonists are recommended to reduce morbidity and mortality following an acute MI in patients who have LVEF of 40% or less who develop symptoms of HF or who have a history of diabetes mellitus, unless contraindicated. I IIa IIb Harm III Inappropriate use of aldosterone receptor antagonists is potentially harmful because of life-threatening hyperkalemia or renal insufficiency when serum creatinine greater than 2.5 mg/dL in men or greater than 2.0 mg/dL in women (or estimated glomerular filtration rate <30 mL/min/1.73m2), and/or potassium above 5.0 mEq/L. Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III The combination of hydralazine and isosorbide dinitrate is recommended to reduce morbidity and mortality for patients self-described as African Americans with NYHA class III–IV HFrEF receiving optimal therapy with ACE inhibitors and beta blockers, unless contraindicated. I IIa IIb III A combination of hydralazine and isosorbide dinitrate can be useful to reduce morbidity or mortality in patients with current or prior symptomatic HFrEF who cannot be given an ACE inhibitor or ARB because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated. Pharmacological Treatment for Stage C HFrEF (cont.) I IIa IIb III Digoxin can be beneficial in patients with HFrEF, unless contraindicated, to decrease hospitalizations for HF. I IIa IIb III Patients with chronic HF with permanent/persistent/ paroxysmal AF and an additional risk factor for cardioembolic stroke (history of hypertension, diabetes mellitus, previous stroke or transient ischemic attack, or ≥75 years of age) should receive chronic anticoagulant therapy (in the absence of contraindications to anticoagulation). Pharmacological Treatment for Stage C HFpEF (cont.) I IIa IIb III I IIa IIb III Management of AF according to published clinical practice guidelines in patients with HFpEF is reasonable to improve symptomatic HF. The use of beta-blocking agents, ACE inhibitors, and ARBs in patients with hypertension is reasonable to control blood pressure in patients with HFpEF. Medical Therapy for Stage C HFrEF: Magnitude of Benefit Demonstrated in RCTs GDMT ACE inhibitor or ARB Beta blocker Aldosterone antagonist Hydralazine/nitrate (Standardized to 36 mo) RR Reduction in HF Hospitalizations 17% 26 31% 34% 9 41% 30% 6 35% 43% 7 33% RR Reduction in Mortality NNT for Mortality Reduction Treatment of Stages A to D Treatment for Stage C HFpEF Treatment of HFpEF Recommendations Systolic and diastolic blood pressure should be controlled according to published clinical practice guidelines Diuretics should be used for relief of symptoms due to volume overload Coronary revascularization for patients with CAD in whom angina or demonstrable myocardial ischemia is present despite GDMT Management of AF according to published clinical practice guidelines for HFpEF to improve symptomatic HF Use of beta-blocking agents, ACE inhibitors, and ARBs for hypertension in HFpEF ARBs might be considered to decrease hospitalizations in HFpEF Nutritional supplementation is not recommended in HFpEF COR LOE I B I C IIa C IIa C IIa C IIb B III: No Benefit C Treatment of Stages A to D Device Treatment for Stage C HFrEF Device Therapy for Stage C HFrEF I IIa IIb III ICD therapy is recommended for primary prevention of SCD to reduce total mortality in selected patients with nonischemic DCM or ischemic heart disease at least 40 days post-MI with LVEF of 35% or less, and NYHA class II or III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for more than 1 year. I IIa IIb III NYHA Class III/IV I IIa IIb III NYHA Class II CRT is indicated for patients who have LVEF of 35% or less, sinus rhythm, left bundle-branch block (LBBB) with a QRS duration of 150 ms or greater, and NYHA class II, III, or ambulatory IV symptoms on GDMT. Treatment of Stages A to D Stage D Clinical Events and Findings Useful for Identifying Patients With Advanced HF Repeated (≥2) hospitalizations or ED visits for HF in the past year Progressive deterioration in renal function (e.g., rise in BUN and creatinine) Weight loss without other cause (e.g., cardiac cachexia) Intolerance to ACE inhibitors due to hypotension and/or worsening renal function Intolerance to beta blockers due to worsening HF or hypotension Frequent systolic blood pressure <90 mm Hg Persistent dyspnea with dressing or bathing requiring rest Inability to walk 1 block on the level ground due to dyspnea or fatigue Recent need to escalate diuretics to maintain volume status, often reaching daily furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone therapy Progressive decline in serum sodium, usually to <133 mEq/L Frequent ICD shocks Adapted from Russell et al. Congest Heart Fail. 2008;14:316-21. Treatment of Stages A to D Water Restriction Water Restriction I IIa IIb III Fluid restriction (1.5 to 2 L/d) is reasonable in stage D, especially in patients with hyponatremia, to reduce congestive symptoms. Surgical/Percutaneous/Transcatheter Interventional Treatment of HF I IIa IIb III I IIa IIb III Coronary artery revascularization via CABG or percutaneous intervention is indicated for patients (HFpEF and HFrEF) on GDMT with angina and suitable coronary anatomy, especially for a left main stenosis (>50%) or left main equivalent disease. CABG to improve survival is reasonable in patients with mild to moderate LV systolic dysfunction (EF 35% to 50%) and significant (≥70% diameter stenosis) multivessel CAD or proximal LAD coronary artery stenosis when viable myocardium is present in the region of intended revascularization. Heart failure with preserved EF or diastolic heart failure Heart failure with preserved EF Case scenario 2 • A 55 yo man presents with gradually increasing shortness of breath and leg swelling that occurred while on a business trip. He has congestive heart failure, which has caused fatigue and shortness of breath if he walks a block or climbs a flight of stairs. BP is 140/ 90; there is no jugular venous distension or gallop, and only minimal pedal edema. AN echo shows left ventricular EF 45 %. Current medication include aspirin and simvastatin. The patient desires to keep medications to a minimum. What additional treatments are indicated at this time? • A. Spironolactone • B. ACE inhibitor and beta blocker • C. Digoxin • D. Frusemide • E. An implantable defibrillator Cardiac rehabilitation • Coordinated interventions designed to optimize a cardiac patient’s physical, psychological, and social functioning, in addition to stabilizing or slowing the progress of underlying atherosclerotic process, thereby reducing morbidity and mortality. • Answer is B • ACE inhibitor is recommended in both symptomatic n asymptomatic heart failure • Beta blocker stabilize left ventricular remodeling • Spironolactone recommended for NYHA III-IV with EF <35% despite on loop diuretic + ACEi + b blocker • Frusemide can improve SSx but patient wants to keep medication to minimal • Defibrillator not indicated yet Cardiac rehabilitation • Include – baseline patient assesssment, – nutritional counselling, – aggressive risk factor management ie • lipid, hpt, weight, diabetes and smoking, – psychosocial and vocational counseling , and – physical activity counseling and exercise training, in addition to – appropriate use of cardioprotective drugs that have evidence-based efficacy for secondary prevention Who should be included in cardiac rehab ? • • • • • Patient with previous MI Who had undergone CABG Those with PCI done Heart transplant candidate or recipient Who has stable chronic heart failure, peripheral arterial disease Exercise training intervention Return to work Cardioprotective mechanism (improve endothelial function) Risk factor modification & intervention Aggresive reduction of risk factors via nutritional counselling, weight management, adherence to drug therapy Psychosocial intervention (address depression, anxiety, social isolation. Consider SSRI, cognitive behavioral therapy. Thank you for your kind attention