Transcript Pharmacologic and Nonpharmacologic Treatments of Ischemic

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???????????????