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PHARMACOLOGIC AND NONPHARMACOLOGIC TREATMENTS OF ISCHEMIC CARDIOMYOPATHY (ICM) PRESENTED BY: MARTHA DRAKE FNP, BC CHICAGO HEART AND VASCULAR ASSOCIATES PURDUE UNIVERSITY CALUMET STUDENT (DNP PROGRAM) LEARNING OBJECTIVES • Describe the pharmacologic treatments of ICM • Discuss the nonpharmacologic treatments of ICM (ICD, Life Vest) • Discuss diagnostic tests to diagnose ICM WHAT IS CARDIOMYOPATHY? • Cardiomyopathy refers to diseases of the heart muscle. • These diseases have many causes, signs and symptoms, and treatments. • In cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid. • In rare cases, the muscle tissue in the heart is replaced with scar tissue. • As cardiomyopathy worsens, the heart becomes weaker. • The heart develops an inability to pump blood through the body and maintain a normal electrical rhythm. This can lead to heart failure or irregular heartbeats called arrhythmia (Ventricular in origin) Source: http://www.nhlbi.nih.gov/health/health-topics/topics/cm/ YOUR HEART IS LIKE A HOUSE • Plumbing; coronary arteries • Electricity: arrhythmia • Sump pump: Left ventricle TYPES OF CARDIOMYOPATHY ISCHEMIC CARDIOMYOATHY (ICM) • Ischemic cardiomyopathy (CM) is the most common type of dilated cardiomyopathy. • ICM is caused by a lack of blood supply to the heart muscle caused by coronary artery disease • In Ischemic CM, the heart's ability to pump blood is decreased because the the left ventricle (sump pump), is enlarged, dilated and weak. • We refer to blockage in the heart as “stenosis” NEW YORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION OF HEART FAILURE Normal daily activity does not initiate symptoms. II Normal daily activities initiate onset of symptoms, but symptoms subside with rest. III Minimal activity initiates symptoms; patients are usually symptom-free at rest. IV Any type of activity initiates symptoms, and symptoms are present at rest. LET’S LOOK AT A CASE STUDY………………. • S.V. is a 56 year old male with the following complaints: • PMH: Type II Diabetes, Hypertension, Hyperlipidemia, Obesity with BMI 36% • Labs: • 25# weight gain in 6 mos • A1C: 10% • CBC: unremarkable • Complains of dyspnea with minimal exertion with “chest tightness” to PCP: onset of symptoms has been increasing over last 3 mos • TSH: unremarkable • Chem 12: unremarkable • FLP: Total cholesterol 231 • “Tired all of the time’ • Trigs: 256 (Bad) • LDL: 138 (Ugly) • HDL: 36 (Good) REFERRAL TO CARDIOLOGY………. • Physical exam • Review of medication • • Is on Janumet for Diabetes • Aggressive management of Lipids • Bruce protocol • Statin therapy has been broadly implicated in prevention of adverse cardiovascular events • Modified Bruce Protocol • Originally designed to lower cholesterol in patients with cardiovascular disease, statins are increasingly recognized for their favorable effects on inflammation, oxidative stress, and vascular performance. • Is on Pravastatin 20mg po daily already • Switch to another statin; Rovustatin or Atorvastatin 12 lead EKG (assess for ST/T wave changes, LVH, LBBB) • Echocardiogram (assesses Ejection fraction (EF): normal is 60-65% • Cardiac Stress or Lexiscan: • Lexiscan • Screening tool • Stress testing provides information about how your heart works during physical stress. Monitors for EKG changes (ST Depression or elevations) NEXT STEP…… • 2 week Follow Up Visit: • Review of echocardiogram: • EF 30% • Schedule for Right and Left heart catheterization to assess for Coronary Artery Disease (CAD) • CAD: • Stenosis of 70% or greater warrants a coronary stent • Atherosclerotic plaque narrows lumen of artery • Chronic inflammatory disorder • Plaque rupture and coronary thrombosis • Plaque regression is possible with change in risk factors • ASA • Statins PHARMACOLOGIC MANAGEMENT: ACC GUIDELINES: HTTP://CONTENT.ONLINEJACC.ORG/ARTICLE.ASPX?ARTICLEID=1695825&_GA=1.140027124. 652429422.1459208354 PHARMACOLOGY CONTINUED: DIURETICS • Diuretics inhibit the reabsorption of sodium or chloride at specific sites in the renal tubules. • Bumetanide, furosemide, and torsemide act at the loop of Henle (thus, the term loop diuretics) • Thiazides, metolazone, and potassium-sparing agents (e.g., spironolactone) act in the distal portion of the tubule • Loop diuretics have emerged as the preferred diuretic agents for use in most patients with HF. • Thiazide diuretics may be considered in hypertensive patients with HF and mild fluid retention because they confer more persistent antihypertensive effects. • Controlled trials have demonstrated the ability of diuretic drugs to increase urinary sodium excretion and decrease physical signs of fluid retention in patients with HF ANGIOTENSIN CONVERTING ENZYME (ACE) AND ANGIOTENSIN RECEPTOR BLOCKERS (ARBS) • ACE Inhibitors: Recommendation • • Class I1: ACE inhibitors are recommended in patients with HFrEF and current or prior symptoms, unless contraindicated, to reduce morbidity and mortality (Level of Evidence: A) The available data suggest that there are no differences among available ACE inhibitors in their effects on symptoms or survival • Treatment with an ACE inhibitor should be initiated at low doses followed by gradual dose increments if lower doses have been well tolerated. • Renal function and serum potassium should be assessed within 1 to 2 weeks of initiation of therapy and periodically thereafter, especially in patients with preexisting hypotension, hyponatremia, diabetes mellitus, azotemia, or in those taking potassium supplements. • ARBs: Recommendations • Class I1. ARBs are recommended in patients with HFrEF with current or prior symptoms who are ACE inhibitor intolerant, unless contraindicated, to reduce morbidity and mortality(Level of Evidence: A) • Class IIa. 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 (Level of Evidence: A) ACE AND ARB EXAMPLES Initial Daily Dose(s) Maximum Dose(s) Mean Doses Achieved in Clinical Trials Captopril 6.25 mg 3 times 50 mg 3 times 122.7 mg/d (422) Enalapril 2.5 mg twice 10 to 20 mg twice 16.6 mg/d (413) Fosinopril 5 to 10 mg once 40 mg once N/A Lisinopril 2.5 to 5 mg once 20 to 40 mg once 32.5 to 35.0 mg/d (445) Perindopril 2 mg once 8 to 16 mg once N/A Quinapril 5 mg twice 20 mg twice N/A Ramipril 1.25 to 2.5 mg once 10 mg once N/A Trandolapril 1 mg once 4 mg once N/A Candesartan 4 to 8 mg once 32 mg once 24 mg/d (420) Losartan 25 to 50 mg once 50 to 150 mg once 129 mg/d (421) Valsartan 20 to 40 mg twice 160 mg twice 254 mg/d (108) ACE inhibitors ARBs SIDE EFFECTS • Angioedema occurs in <1% of patients who take an ACE inhibitor, but it occurs more frequently in blacks. • Because its occurrence may be life-threatening, clinical suspicion of this reaction justifies the subsequent avoidance of all ACE inhibitors for the lifetime of the patient. • ACE inhibitors should not be initiated in any patient with a history of angioedema. • Although ARBs may be considered as alternative therapy for patients who have developed angioedema while taking an ACE inhibitor, there are some patients who have also developed angioedema with ARBs, and caution is advised when substituting an ARB in a patient who has had angioedema associated with use of an ACE inhibitor • ACE cough occurs in 20% of patients on therapy • Dizziness • Hypotension • Hyperkalemia • Renal Dysfunction BETA BLOCKERS • Beta Blockers: Recommendation • Class I1. • Use of 1 of the 3 beta blockers proven to reduce mortality (e.g., 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 (Level of Evidence: A) • Three beta blockers have been shown to be effective in reducing the risk of death in patients with chronic HFrEF: bisoprolol and sustainedrelease metoprolol (succinate), which selectively block beta-1–receptors; and carvedilol, which blocks alpha-1–, beta-1–, and beta-2–receptors. • Beta blockers should be prescribed to all patients with stable HFrEF unless they have a contraindication to their use or are intolerant of these drugs. Because of its favorable effects on survival and disease progression, a clinical trial– proven beta blocker should be initiated as soon as HFrEF is diagnosed. BETA BLOCKER SIDE EFFECTS • Initiation of treatment with a beta blocker may produce adverse reactions that require attention and management: • Fluid retention and worsening HF; • Fatigue; • Bradycardia or heart block • Dizziness • Hypotension. • Depression BETA BLOCKERS Beta blockers Bisoprolol 1.25 mg once 10 mg once 8.6 mg/d (117) Carvedilol 3.125 mg twice 50 mg twice 37 mg/d (447) Carvedilol CR 10 mg once 80 mg once N/A Metoprolol succinate extended release (metoprolol CR/XL) 12.5 to 25 mg once 200 mg once 159 mg/d (448) ALDOSTERONE RECEPTOR ANTAGONISTS • Aldosterone Receptor Antagonists: Recommendations • Class I1.Aldosterone receptor antagonists (or mineralocorticoid receptor antagonists) are recommended in patients with NYHA class II–IV HF and who have LVEF of 35% or less unless contraindicated, to reduce morbidity and mortality. • Patients with NYHA class II HF should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists. • Creatinine should be 2.5 mg/dL or less in men or 2.0 mg/dL or less in women (or estimated glomerular filtration rate >30 mL/min/1.73 m2), and potassium should be less than 5.0 mEq/L. • Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation and closely followed thereafter to minimize risk of hyperkalemia and renal insufficiency(Level of Evidence: A) • The landmark RALES trial (Randomized Aldactone Evaluation Study) showed a 30% reduction in allcause mortality as well as a reduced risk of SCD and HF hospitalizations with the use of spironolactone in patients with chronic HFrEF and LVEF <35%. • Eplerenone has been shown to reduce all-cause deaths, cardiovascular deaths, or HF hospitalizations in a wider range of patients with HFrEF DRUG DOSING FOR ALDOSTERONE RECEPTOR ANTAGONISTS Eplerenone Spironolactone eGFR (mL/min/1.73 m2) ≥50 30 to −49 Initial dose (only if K+ ≤5 mEq/L) 25 mg once every other 12.5 to 25.0 mg once day daily 12.5 mg once daily or every other day 25 mg once or twice daily 12.5 to 25.0 mg once daily 25 mg once daily Maintenance dose (after 50 mg once daily 4 wk for K+ ≤5 mEq/L)∗ 25 mg once daily ≥50 30 to 49 HYDRALAZINE AND ISOSORBIDE DINITRATE • Hydralazine and Isosorbide Dinitrate: Recommendations • Class I1.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. (Level of Evidence: A) • Class IIa. 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 (Level of Evidence: B) DIGOXIN • Digoxin: Recommendation • Class Iia: Digoxin can be beneficial in patients with HFrEF, unless contraindicated, to decrease hospitalizations for HF(Level of Evidence: B) • Several placebo-controlled trials have shown that treatment with digoxin for 1 to 3 months can improve symptoms, HRQOL, and exercise tolerance in patients with mild to moderate HF • These benefits have been seen regardless of the underlying rhythm (normal sinus rhythm or AF), cause of HF (ischemic or nonischemic cardiomyopathy), or concomitant therapy (with or without ACE inhibitors). • In a long-term trial that primarily enrolled patients with NYHA class II or III HF, treatment with digoxin for 2 to 5 years had no effect on mortality but modestly reduced the combined risk of death and hospitalization CALCIUM CHANNEL BLOCKERS • No benefit per ACC guidelines • Cardizem • Verapamil • Norvasc 2 WEEKS AFTER THE ANGIOGRAM FOLLOW-UP VISIT • s/p Drug-Eluting Stent (DES) to mid LAD and mid RCA • Plavix (Clopridogrel) 75mg po daily • Clopidogrel is an antiplatelet agent used to reduce the risk of myocardial infarction (MI) and stroke among high-risk patients. • It is also approved for secondary prevention of atherosclerotic events for patients who have recently had an MI or a stroke and those with established peripheral arterial disease, and administered with aspirin as dual antiplatelet therapy (DAPT) for patients with acute coronary syndrome (ACS) caused by an MI or unstable angina. • CYP2C19 is one of the principal enzymes involved in the hepatic bioactivation of clopidogrel. • But because it has to be processed and activated in the liver, it sometimes takes a while for Plavix to take effect • Some people do not, in fact, respond to Plavix at all. Only a genetic test—which requires additional time and expense for the patient—can tell if a person has a variant on the CYP2C19 gene that affects the way Plavix works. • EF 30% per LV gram • Pharmacologic Therapy: • ACE/BB/Statin/ASA/Lasix: continue titration to toleration • Addition of Antiplatelet therapy: in this patient: Plavix OTHER OPTIONS FOR ANTIPLATELET THERAPY • Brilinta: (Ticagrelor) • Initiate treatment with a 180 mg (two 90 mg tablets) loading dose given orally and continue treatment with 90 mg orally twice daily. After the initial loading dose of aspirin (usually 325 mg), use a daily maintenance dose of aspirin of 81mg • Maintenance doses of aspirin above 100 mg decreased the effectiveness of Brilinta. Avoid maintenance doses of aspirin above 100 mg daily. • Brilinta (approved in 2011) has been found to be more effective than Plavix, and it also begins working more quickly than this older drug because it also doesn’t have to be processed in the liver • No genetic testing is required, since Brilinta isn’t affected by the gene variant that interferes with Plavix. • The downside of this, though, is that Brilinta wears off more quickly because the drug doesn’t bind to platelets permanently like Plavix and Effient. People must also take a low-dose aspirin (81 mg per day) along with Brilinta to get this greater level of effectiveness, though many people who take Plavix are also on a low-dose aspirin regimen already. • Brilinta must be taken twice a day rather than once a day like Plavix. Some people also experience shortness of breath with Brilinta, particularly in the first few weeks of taking it, and they must be switched to one of the other two medications EFFIENT • Effient (Prasugrel) • COST!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! • Initiate treatment as a single 60 mg oral loading dose and then continue at 10 mg orally once daily. Patients should also take aspirin (75 mg to 325 mg) daily • Effient and Brilinta are expensive!!!!!!!!!!!!!!!!!!!!!!!! • Effient (approved in 2009) has been found to be more effective than Plavix and it works more quickly because it doesn’t have to go through the metabolic pathway that Plavix does. • There’s no need for genetic testing to see if the Effient will work. • However, a study published in the New England Journal of Medicine of 13,000 patients suggested that there are higher risks of internal bleeding—some fatal—with Effient. Some experts believe this increased bleeding risk basically cancels out the drug’s benefits. IMPLANTABLE CARDIOVERTER DEFIBRILLATOR DISUCUSSION • This is when you have to initiate conversation about an ICD implant • Patient needs to continue pharmacologic therapy • Repeat Echocardiogram in 3 mos • If EF does not increase greater than 3035% then they are a candidate for an ICD • Cardiac Rehab • Boston Scientific • Medtronic • St. Jude • Biotronik ICD THERAPY • Device Therapy for Stage C HFrEF: Recommendations • Class I1.ICD therapy is recommended for primary prevention of SCD to reduce total mortality in selected patients with nonischemic CM 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† ICD GUIDELINES ZOLL LIFEVEST • The Zoll LifeVest AED is unique in that it offers the consistent comfort and serenity in knowing that it is the first FDA-approved (circa 2002) wearable defibrillator. The peace-of-mind of knowing that if and when a patient whom suffers from Sudden Cardiac Arrest (SCA) will always have an on-hand solution if anything were to present itself without warning. It is a non-intrusive resolution to a cardiac patient’s every worry. A simple concept as a wearable defibrillator such as the Zoll LifeVest has the capability to save lives within an instant. EXTRAS Surface of Left Ventricle Electrocardiographic Leads Coronary Artery Usually Involved Inferior II, III, aVF Right coronary artery Lateral V5-V6, I, aVL Left circumflex Anterior V2-V4 Left anterior descending Anterior lateral V1-V6, I, aVL Left main coronary artery Septal V1-V2 Left anterior descending Posterior V1-V2 Left circumflex or right coronary artery (reciprocal changes) SOURCES • http://www.nhlbi.nih.gov/health/healthtopics/ • http://www.lifevest.zoll.com/ • http://www.healthcentral.com/heartdisease/c/978365/147005/brilinta • http://content.onlinejacc.org/article.aspx? articleid=1695825&_ga=1.126396618.65 2429422.1459208354 QUESTIONS???????????????