Guidelines for the Management of Post-MI Patients in the Outpatient Settings
Ramaz Mitaishvili, MD
Gina Gagua, LAc, PhD
Introduction
Compelling clinical trial evidence exists that antiplatelet, ß-blocker, angiotensin-converting enzyme (ACE) inhibitor, and lipid-lowering therapies reduce the risk of recurrent cardiovascular events, hospitalization, and heart failure and substantially improve survival in Post MI patients. Despite this evidence as well as clinical guidelines recommending these cardiovascular protective treatments in Post MI patients, a number of studies have documented low treatment rates in this patient population. The conventional approach to the initiation of lipid-lowering therapy was to not start therapy in the hospital for patients with acute MI; instead, the many practitioners recommended waiting a period of time until the patient was metabolically stable as an outpatient.
Abstract
We summarized both the evidence and expert opinion and provide final recommendations for patient evaluation and therapy. Be aware, that usefulness/efficacy of this guideline in some cases should be in accordance with physician’s opinion, intuition, and knowledge as well as with personal experience.
A complete list of the thousands of publications on various aspects of this subject is beyond the scope of these Guidelines; only selected references are included.
To achieve constant improvement of Guidelines we encouraging providers to complete PMIW (post-MI Worksheet), designed to educate patients, care- givers and to collect important evidence-based information, progress, and statistic for further evaluation to improve post-MI care in Outpatient Clinic or Physician’s Office.
Potential barriers to the implementation of the guideline would be as follows:
Lack of resources and facilities.
Lack of access to diagnostic equipment including electrocardiogram machine within some outpatient’s clinics.
Lack of specialist-generalist communication; passing on of responsibility.
Increased prescribing costs. Inadequate prescription-medication benefits, restrictive formularies.
Focus of physicians on acute problems.
Time constraints and lack of incentives, including lack of reimbursement.
Lack of physician training, including inadequate knowledge of benefits and lack of prescription experience.
Guidelines that call for delaying.
Cardiovascular Risk Following MI
The cardiovascular risk after acute MI remains substantial. Patients with a prior history of MI are five to seven times more likely to sustain a cardiovascular event than are individuals without clinically evident atherosclerotic vascular disease. These post-infarction patients remain at risk for recurrent events even if they are entirely asymptomatic, have no demonstrated ischemia on stress testing, and have undergone complete revascularization. Patients after acute MI thus constitute a very high-risk group for recurrent cardiovascular events, hospitalizations, heart failure, and cardiovascular mortality. One of the major cause of Sudden Cardiac Death are SCD to tachyarrhythmic events after a recent myocardial infarction (MI). Another cause of recurrent events is patients non-compliance due to post-MI depression, and other disorders (primary or secondary).
Criteria for Specialist Referral
Outpatient practitioner must be ready for specialist referral and develop individual strategy for each post-MI patient.
1. Patients who have had a recent onset chest pain in the last 2 – 4 weeks should be referred to the Hospital.
2. Patients who have had previous assessment of chest pain in either the Cardiology clinic, A & E department or as an inpatient or outpatient, should be referred to the Cardiology Outpatient clinic in the normal way.
3. Patients suspected of having acute and severe pain in the background of stable angina should be referred to the A & E department as they could be
suffering from MI/unstable angina.
4. Except under exceptional circumstances, women under 40 and men under 30 should not be referred to the Hospital, because the probability of coronary heart disease in these groups is extremely low.
5. Patients with abnormal ECG’s are at greatest risk and should be considered for specialist referral.
6. Patients with chest pain and murmurs suggesting aortic stenosis should be considered for specialist referral.
7. Patients where clinical condition gives rise for concern, e.g. failure to respond to management/ treatment outlined in this guideline, pain at rest or at night, concurrent illnesses, particularly diabetes, should be considered for specialist referral.
8. Patient with signs and symptoms of post-MI Depression should be considered for specialist referral.
Indications for ICD therapy from the ACC/AHA Task Force on Practice Guidelines and endorsed by the North American Society for Pacing and Electrophysiology
Cardiac arrest due to VF or VT not due to transient or reversible causes
Spontaneous, sustained VT with structural heart disease
Syncope with inducible, sustained, hemodynamically significant VT of VF, when drug therapy is not effective, tolerated, or preferred
Nonsustained VT with coronary artery disease, prior MI, LV dysfunction, and inducible VF or sustained inducible VT not suppressible with a class I antiarrhythmic
Spontaneous, sustained VT without structural heart disease, not amenable to other treatments
Treatment and Follow-up of the Post-MI patients
The Aims of the Outpatient practitioner
To achieve and maintain patients’ BP at or less than 140/85 mmHg
To achieve and maintain optimum control of blood pressure and glucose for diabetic patients
To achieve and maintain patients’ total cholesterol level at or less than 100 mg/dL
To achieve and maintain 100% of patients not smoking
To advise on lifestyle modification, eg. Diet, management of obesity, alcohol consumption, exercise, and community physical activity programs, reinforced with appropriate literature
To make referrals to specialist services where appropriate, eg. Dietitian, smoking
cessation clinics
To check compliance and patients’ understanding of current pharmacological
intervention (see recommendations below)
To check and discuss general health issues with patients
Pharmacological Intervention
Today, post-MI patients are typically treated with thrombolytic therapy and revascularization procedures. Recovery is usually followed by cardiac rehabilitation, counseling on diet and lifestyle changes, and pharmacologic therapy, including aspirin, statins, blockers, angiotensin-converting enzyme (ACE) inhibitors and, in some cases, antiarrhythmic agents. Current American Heart Association (AHA)/American College of Cardiology (ACC) guidelines recommend class 1 indications for aspirin therapy in all post-MI patients; statins in all patients with low-density lipoprotein cholesterol greater than 100 mg/dL; ßblocker therapy in all but either the lowest-risk patients or those with a clear contraindication; and ACE inhibitors in patients with prior MI and either ejection fraction (EF) less than 40% or congestive heart failure.
Aspirin should be given routinely to and continued for life in patients A with CHD – a dose of 75-150 mg aspirin per day is recommended in post MI patients
Clopidogrel (75 mg/day) is an effective alternative in patients A with contraindications to aspirin, or who are intolerant of aspirin.
Caution should be exercised in the use of Clopidogrel, which can A cause GI upset in some patients.
β-blocker therapy should be given to patients following myocardial infarction unless there are contraindications
Long term ACE inhibitor therapy should be given to patients A following MI with or without left ventricular dysfunction, unless there are contraindications
In post MI patients with left ventricular dysfunction, ACE inhibitor A therapy should be considered within 48 hours of the onset of symptoms – refer to guidelines for the management of heart failure
Caution should be exercised in the use of ACE inhibitors in patients who are hypotensive, who have moderate renal failure, or who are known to have renal artery stenosis.
The initiation of Statin therapy should be considered in accordance of guidelines.
Benefits of Cardiovascular Protective Medications
As stated above, compelling evidence exists that antiplatelet therapy, ßblockers, ACE inhibitors, and lipidlowering therapy each reduce the risk of recurrent cardiovascular events, hospitalizations, heart failure, and mortality in patients following MI.
Each of these therapies individually has been demonstrated to have early as well as long-term benefits in patients presenting with MI.
Lipidlowering Medications Side Effect
We received tenth of adverse reports of patients receiving Lipidlowering medications. Statins can cause chronic aches and pains, liver inflammation, myopathy, numbness, weakness, confusion, fatigue, statin amnesia and other forms of memory dysfunction, hostility, aggression and profound depression, loss of libido and impotence, shortness of breath and even heart failure.
This chapter describes possible adverse of statins. Reports about adverse effects of statins are increasing dramatically, but they still vast minority. More reports have praised statins. We don’t have to speculate by reporting about negative or positive sides of cholesterol lowering medications. Another medications described above also characterized by some adverse effects, but they are minor compare to advantages. With lipidlowering drugs, each case must be evaluated individually, because cholesterol lowering medications can be replaced by some supplements. We strongly recommend to all outpatient physicians do not ignore any negative reports from post-MI patients about prescribed medications, because physicians have such a difficult time believing that their physical problems might be an adverse effect of those drugs. There will be no “conflict of interest” with guidelines, because we all have only interest- to help patients fight them condition. In addition be aware, that almost all lipidlowering medications are statins (different countries have different names for their statin drugs and many statins will become combined with other chemicals in the near future and assume even different names for patent protection and greater marketability), so replacing one medication by another can only aggravate the condition.
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Conclusions
Despite compelling scientific evidence of the benefits of antiplatelet, ß-blocker, ACE inhibitor, and lipidlowering therapy, a substantial proportion of patients after acute MI are not on treatment with these evidence-based, guideline-recommended therapies. It has been clearly documented that not enough has been done to change this situation. Over half of the patients discharged after MI and lacking relevant contraindications or intolerance were not treated with all four of the key classes of medications. Under conventional management, less than 20% of patients discharged without one or more of the cardiovascular protective medications will be started on these drugs on an outpatient basis. The evidence from recent trials and clinical studies provides a compelling argument for prescribing a combination of cardiovascular protective medications in the hospital as part of a systematic approach to prevent remodeling and address the underlying atherosclerotic vascular disease process. Outpatient-based systems to ensure initiation of cardiovascular protective therapies have been demonstrated to improve treatment rates, long-term patient compliance, and clinical outcomes in patients with acute MI. Widespread application of outpatient-based cardiovascular protective treatment–initiation programs for acute MI could dramatically increase treatment rates with these proven, cost-effective therapies and thus substantially reduce the risk of recurrent cardiovascular events, heart failure, and hospitalizations in the large number of patients hospitalized with acute MI and save many additional lives every year.
Main Points
Following acute myocardial infarction (MI), patients face a high risk of recurrent cardiovascular events, hospitalizations, heart failure, and mortality.
Antiplatelet therapy, ß-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins all reduce cardiovascular risks following acute MI, and their effects are additive.
In-hospital initiation of aspirin, ß-blocker, ACE inhibitor, and lipid-lowering therapy has been shown to improve treatment rates, long-term patient compliance, and clinical outcomes in patients with acute MI and is now recommended as the standard of care in patients with coronary heart disease.
Despite these findings and national guidelines, a substantial proportion of post-MI patients is not receiving these medications.
Reasons for the under-use of these medications include the reluctance of physicians to prescribe ß-blockers to post-MI patients with left ventricular dysfunction and/or symptoms of heart failure; however, recent studies suggest that the ß-blocker carvedilol is safe and effective in these patients.
Widespread implementation of hospital-based cardiovascular protective treatment–initiation programs for acute MI could dramatically increase treatment rates with these therapies and thus substantially reduce the risk of recurrent cardiovascular events, heart failure, and hospitalizations in the large number of patients admitted for acute MI every year.
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Definition of Related Terminology
Acute coronary syndrome—any constellation of clinical
signs or symptoms suggestive of AMI or UA. This
syndrome includes patients with AMI, STEMI,
NSTEMI, enzyme-diagnosed MI, biomarker-diagnosed
MI, late ECG-diagnosed MI, and UA. This term is
useful to generically refer to patients who ultimately prove
to have 1 of these diagnoses to describe management
alternatives at a time before the diagnosis is ultimately
confirmed. This term is also used prospectively to identify
those patients at a time of initial presentation who should
be considered for treatment of AMI or UA. Probable
acute coronary syndrome is a term that is commonly
used, and this represents the primary consideration of
patients on initial presentation. Possible acute coronary
syndrome is useful as a secondary diagnosis when an
alternate diagnosis seems more likely but an acute ischemic
process has not been excluded as a possible cause of
the presenting symptoms.
Acute myocardial infarction—an acute process of myocardial ischemia with sufficient severity and duration to
result in permanent myocardial damage. Clinically, the
diagnosis of permanent myocardial damage is typically
made when there is a characteristic rise and fall in cardiac
biomarkers indicative of myocardial necrosis that may or
1040 Braunwald et al. JACC Vol. 36, No. 3, 2000
ACC/AHA Guidelines for Unstable Angina September 2000:970–1062
may not be accompanied by the development of Q waves
on the ECG. Permanent myocardial damage may also be
diagnosed when histological evidence of myocardial necrosis
is observed on pathological examination.
Angina pectoris—a clinical syndrome typically characterized
by a deep, poorly localized chest or arm discomfort
that is reproducibly associated with physical exertion or
emotional stress and relieved promptly (i.e., ,5 min) with
rest or sublingual NTG. The discomfort of angina is often
hard for patients to describe, and many patients do not
consider it to be “pain.” Patients with UA may have
discomfort with all the qualities of typical angina except
that episodes are more severe and prolonged and may
occur at rest with an unknown relationship to exertion or
stress. In most, but not all, patients, these symptoms
reflect myocardial ischemia that results from significant
underlying CAD.
Angiographically significant coronary artery disease—
CAD is typically judged “significant” at coronary angiography
if there is $70% diameter stenosis, assessed visually,
of $1 major epicardial coronary segments or $50%
diameter stenosis of the left main coronary artery. The
term “significant CAD” used in these guidelines does not
imply clinical significance but refers only to an angiographically
significant stenosis.
Coronary artery disease—although a number of disease
processes other than atherosclerosis can involve coronary
arteries, in these guidelines, the term “CAD” refers to the
atherosclerotic narrowing of the major epicardial coronary
arteries.
Enzyme- or biomarker-diagnosed acute myocardial
infarction—diagnostic elevation of cardiac enzymes or
biomarkers (e.g., troponin) that indicates definite myocardial
injury in the absence of diagnostic ECG changes
(Q waves or ST-segment deviation).
Ischemic heart disease—a form of heart disease with
primary manifestations that result from myocardial ischemia
due to atherosclerotic CAD. This term encompasses
a spectrum of conditions, ranging from the asymptomatic
preclinical phase to AMI and sudden cardiac death.
Likelihood—used in these guidelines to refer to the
probability of an underlying diagnosis, particularly significant
CAD.
Myocardial ischemia—a condition in which oxygen delivery to and metabolite removal from the myocardium
fall below normal levels, with oxygen demand exceeding
supply. As a consequence, the metabolic machinery of
myocardial cells is impaired, leading to various degrees of
systolic (contractile) and diastolic (relaxation) dysfunction.
Ischemia is usually diagnosed indirectly through
techniques that demonstrate reduced myocardial blood
flow or its consequences on contracting myocardium.
Non–Q-wave myocardial infarction—an AMI that is
not associated with the evolution of new Q waves on the
ECG. The diagnosis of non–Q-wave MI is often difficult
to make soon after the event and is commonly made only
retrospectively on the basis of elevated cardiac enzyme
levels.
Non–ST-segment elevation myocardial infarction—
NSTEMI is an acute process of myocardial ischemia with
sufficient severity and duration to result in myocardial
necrosis (see Acute Myocardial Infarction). The initial
ECG in patients with NSTEMI does not show STsegment
elevation; the majority of patients who present
with NSTEMI do not develop new Q waves on the ECG
and are ultimately diagnosed as having had a non–Qwave
MI. NSTEMI is distinguished from UA by the
detection of cardiac markers indicative of myocardial
necrosis in NSTEMI and the absence of abnormal
elevation of such biomarkers in patients with UA.
Post–myocardial infarction angina—UA occurring
from 1 to 60 days after an AMI.
Reperfusion-eligible acute myocardial infarction—a
condition characterized by a clinical presentation compatible
with AMI accompanied by ST-segment elevation or
new LBBB or anterior ST-segment depression with
upright T waves on ECG.
Unstable angina—an acute process of myocardial ischemia
that is not of sufficient severity and duration to result
in myocardial necrosis. Patients with UA typically do not
present with ST-segment elevation on the ECG and do
not release biomarkers indicative of myocardial necrosis
into the blood.
Variant angina—a clinical syndrome of rest pain and
reversible ST-segment elevation without subsequent enzyme
evidence of AMI. In some patients, the cause of this
syndrome appears to be coronary vasospasm alone, often
at the site of an insignificant coronary plaque, but a
majority of patients with variant angina have angiographically
significant CAD.
Abbreviations
AAFP American Academy of Family
Physicians
ACC American College of Cardiology
ACE angiotensin-converting enzyme
ACEP American College of Emergency
Physicians
ACEI angiotensin-converting enzyme
inhibitor
ACIP Asymptomatic Cardiac Ischemia
Pilot
ACP-ASIM American College of Physicians–
American Society of Internal
Medicine
ACS acute coronary syndrome
ACT activated clotting time
JACC Vol. 36, No. 3, 2000 Braunwald et al. 1041
September 2000:970–1062 ACC/AHA Guidelines for Unstable Angina
ADP adenosine diphosphate
AHA American Heart Association
AHCPR Agency for Health Care Policy
and Research
AMI acute myocardial infarction
aPTT activated partial thromboplastin
time
ASA aspirin
ATACS Antithrombotic Therapy in
Acute Coronary Syndromes
AV atrioventricular
BARI Bypass Angioplasty
Revascularization Investigation
CABG coronary artery bypass graft
surgery
CABRI Coronary Angioplasty versus
Bypass Revascularisation
Investigation
CAD coronary artery disease
CAPRIE Clopidogrel versus Aspirin in
Patients at Risk of Ischaemic
Events
CAPTURE c7E3 Fab Antiplatelet Therapy
in Unstable Refractory Angina
CARS Coumadin Aspirin Reinfarction
Study
CASS Coronary Artery Surgery Study
CCS Canadian Cardiovascular Society
CHAMP Combination Hemotherapy And
Mortality Prevention
cGMP cyclic guanosine monophosphate
CHF congestive heart failure
CI confidence interval
CK creatine kinase
CLASSICS CLopidogrel ASpirin Stent
International Cooperative Study
COPD chronic obstructive pulmonary
disease
CRP C-reactive protein
cTnI cardiac-specific TnI
cTnT cardiac-specific TnT
CURE Clopidogrel in Unstable angina
to Prevent ischemic Events
DANAMI DANish trial in Acute
Myocardial Infarction
DATA Diltiazem as Adjunctive Therapy
to Activase
DAVIT Danish Study Group on
Verapamil in Myocardial Infarction
DRS Diltiazem Reinfarction Study
DTS Duke Treadmill Score
EAST Emory Angioplasty versus
Surgery Trial
ECG 12-lead electrocardiogram,
electrocardiographic
ED emergency department
EF ejection fraction (left ventricle)
EPIC Evaluation of c7E3 for the
Prevention of Ischemic
Complications
EPILOG Evaluation of PTCA to Improve
Long-term Outcome by c7E3
GPIIb/IIIA receptor blockade
EPISTENT Evaluation of Platelet IIb/IIIa
Inhibitor for STENTing
ESSENCE Efficacy and Safety of
Subcutaneous Enoxaparin in
Non–Q wave Coronary Events
FRAXIS FRAxiparine in Ischaemic
Syndrome
FRIC FRagmin In unstable Coronary
artery disease study
FRISC Fragmin during Instability in
Coronary Artery Disease
FRISC II Fast Revascularization During
Instability in Coronary Artery
Disease
GABI German Angioplasty Bypass
Surgery Investigation
GISSI-1 Gruppo Italiano per lo Studio
della Sopravvivenza nell’Infarto-1
GISSI-3 Gruppo Italiano per lo Studio
della Sopravvivenza nell’infarto
Miocardico
GP glycoprotein
1042 Braunwald et al. JACC Vol. 36, No. 3, 2000
ACC/AHA Guidelines for Unstable Angina September 2000:970–1062
GUSTO-II Global Use of Strategies to Open
Occluded Coronary Arteries-II
HDL high-density lipoprotein
HERS Heart and Estrogen/progestin
Replacement Study
HINT Holland Interuniversity Nifedipine/
metoprolol Trial
HOPE Heart Outcomes Prevention
Evaluation
HRT hormone replacement therapy
IABP intra-aortic balloon pump
IMPACT Integrilin to Minimise Platelet
Aggregation and Coronary
Thrombosis
IV intravenous
ISIS International Study of Infarct
Survival
LAD left anterior descending coronary
artery
LBBB left bundle-branch block
LDL low-density lipoprotein
LMWH low-molecular-weight heparin
LV left ventricular, left ventricle
MATE Medicine versus Angiography in
Thrombolytic Exclusion
MDPIT Multicenter Diltiazem Postinfarction
Trial
MET metabolic equivalent
MB cardiac muscle isoenzyme of
creatine kinase
MI myocardial infarction
MM skeletal muscle isoenzyme of
creatine kinase
MR mitral regurgitation
MV˙ O2 myocardial oxygen consumption
NCEP National Cholesterol Education
Program
NHAAP National Heart Attack Alert
Program
NHLBI National Heart, Lung, and Blood
Institute
NSTEMI non–ST-segment elevation
myocardial infarction
NTG nitroglycerin
OASIS Organization to Assess Strategies
for Ischemic Syndromes
OR odds ratio
PCI percutaneous coronary
intervention
PR ECG PR segment
PRISM Platelet Receptor Inhibition in
Ischemic Syndrome Management
PRISM-PLUS Platelet Receptor Inhibition in
Ischemic Syndrome Management
in Patients Limited by Unstable
Signs and Symptoms
PTCA percutaneous transluminal
coronary angioplasty
PURSUIT Platelet Glycoprotein IIb/IIIa in
Unstable Angina: Receptor
Suppression Using Integrilin
Therapy
RESTORE Randomized Efficacy Study of
Tirofiban for Outcomes and
REstenosis
RISC Research Group in Instability in
Coronary Artery Disease
RITA Randomized Intervention
Treatment of Angina
RR relative risk
SHEP Systolic Hypertension in the
Elderly Program
SHOCK SHould we emergently
revascularize Occluded
Coronaries for cardiogenic shocK
STEMI ST-segment elevation myocardial
infarction
STS Society of Thoracic Surgeons
SVG saphenous vein graft
TIMI Thrombolysis In Myocardial Infarction
TIMI 9A and 9B Thrombolysis and Thrombin
Inhibition in Myocardial Infarction
TnC troponin C
TnI troponin I
TnT troponin T
JACC Vol. 36, No. 3, 2000 Braunwald et al. 1043
September 2000:970–1062 ACC/AHA Guidelines for Unstable Angina
TTP thrombotic thrombocytopenia
purpura
UA unstable angina
UFH unfractionated heparin
UKPDS UK Prospective Diabetes Study
VA Veterans Administration
VANQWISH Veterans Affairs Non–Q-Wave
Infarction Strategies in Hospital
WISE Women’s Ischemia Syndrome
Evaluation
©Copyright 2003 by RAMAZ MITAISHVILI. All rights reserved. This article may not be reproduced by any means without the prior written permission of the author.
