Download Acute Myocardial Infarction- The Changing Face

© SUPPLEMENT TO JAPI • december 2011 • VOL. 59 5
Editorial
Acute Myocardial Infarction- The Changing Face
Aspi R Billimoria*, Vaibhav M Dedhia**
M
uch water has flown under the bridge in the diagnosis and
treatment of acute myocardial infarction of yore when
the patient was put to bed for two or three weeks, there was
hardly any treatment apart from pain killers and nitrates and
the value of rehabilitation was something unheard of. This issue
of the journal emphasises the recent advances in the diagnosis,
treatment and rehabilitation.
ST Elevation Myocardial infarction (STEMI) is a major public
health problem in both the developed and the developing
countries in the world. The incidence in the developing countries
is now similar to that in the developed countries.1
Diagnosis of myocardial infarction has two components. A
pathological component which requires evidence of myocyte cell
death as a consequence of prolonged ischaemia and a clinical
diagnosis which requires an assessment of the history with
evidence of infarction using electrocardiographic, biochemical
and imaging modalities. Classically the criteria required the
presence of at least two of the following three criteria to establish
the diagnosis of myocardial infarction: Characteristic symptoms,
electrocardiographic changes and typical rise and fall in the
biochemical markers.2 Since the earlier publications many
advances in the laboratory and electrocardiographic aspects
of the definition have occurred. The assays for biochemical
parameters have become more specific. Keeping this in mind
a consensus document with regard to the revised definition
of acute myocardial infarction was published jointly by the
European society of cardiology and the American College of
Cardiology.3
Revised Definition of Myocardial
Infarction (Mi)3
Criteria for acute, evolving or recent MI
Either one of the following criteria satisfies the diagnosis for
an acute, evolving or recent MI
1. Typical rise and gradual fall (troponin) or more rapid rise
and fall (CPK-MB) of biochemical markers of myocardial
infarction with at least one of the following:
a.
b. Development of pathologic Q waves on the ECG
reading
Ischaemic symptoms
c.
d. Coronary artery intervention (e.g. Coronary angioplasty)
ECG changes indicative of ischaemia (St segment
elevation or depression)
2. Pathological findings of acute MI
Criteria for established MI
Either of the following criteria satisfies the diagnosis for
established MI:
Former Head, Department of Cardiology, St. George’s Hospital and
Grant MedicalCollege, Mumbai; Cardiologist, Conwest and Manjula
S. Badani Hospital, Mumbai; **Interventional Cardiologist: Prince
Aly Khan Hospital, Cumballa Hill Hospital-Mumbai; Cardiologist:
Conwest and Manjula S. Badani Hospital.
*
1. Development of new pathological Q waves on serial ECG
readings. The patient may or may not remember previous
symptoms. Biochemical markers of myocardial necrosis may
have normalised, depending on the length of time that has
passed since the infarct developed.
2. Pathological findings of a healed infarct or healing MI. In this
issue Wander has drawn attention to a correct diagnosis after
proper history taking. He has stressed on the difficulties in
diagnosing infarction in the presence of Left Bundle Branch
Block and on the newer modalities of diagnosis.
Prehospital Thrombolysis
STEMI is fatal in about one third of the patients, with
50% deaths occurring in the first hour from ventricular
tachyarrhythmias. Time to thrombolysis remains a key
modifiable determinant of mortality in STEMI. 4,5 A prehospital treatment strategy when compared with in-hospital
thrombolysis has been shown to reduce time to thrombolysis
with around one hour and in-hospital mortality by 17% in a metaanalysis of randomized trials.6 A nationwide registry (>13000
patients) of real-life patients showed that prehospital diagnosis
and treatment are associated with reduced time to thrombolysis
by almost 1 h and reduced adjusted long-term mortality by 30%.
Importantly, prehospital diagnosis established by a physician
at the hospital using telemedicine and subsequent pre hospital
thrombolysis (PHT) delivered by paramedics in the ambulances
seem as efficient in reducing time delays as physician-staffed
ambulances.7 The results of a nationwide prospective registry
of patients admitted to intensive care units for acute myocardial
infarction in November 2000 in France show that prehospital
thrombolysis therapy with liberal use of early angioplasty offers
1-year mortality results that are at least as satisfactory as those
with primary coronary angioplasty. In patients treated very
early (those admitted within 3.5 hours of onset of chest pain),
PHT offers superior efficacy compared with any other mode of
reperfusion therapy.8 Here, Vaishnave et al have dealt with the
need for domiciliary thrombolysis and the need for TIMI 3 flow.
They have also pointed out the increased effect by the addition of
aspirin. At the same time they have cautioned the use in NESTMI.
Approach to Stemi and Non STEMI
The ACC and AHA guidelines suggest an approach
that integrates the information from history, examination,
electrocardiogram, cardiac biomarkers to assign the patient to
four categories- noncardiac chest pain, stable angina, possible
acute coronary syndrome or definite acute coronary syndrome.9
In these guidelines, patients with STEMI are triaged
immediately for reperfusion therapy and those with unstable
angina or non ST elevation MI are admitted to hospital for risk
stratification and treated conservatively or an early invasive
strategy is adopted depending on the quantum of risk that is
involved.
6
Thrombolysis in the Era of
Intervention
Once a patient with STEMI presents, then an assessment is
made of the different reperfusion options.10
Step 1: Assess time and risk
•
Time since symptom onset.
•
Risk of STEMI
•
Role of fibrinolysis
•
Time required for transport to a skilled PCI laboratory
Step 2: Determine if fibrinolysis or invasive strategy is
preferred
If presentation is < 3hours and there is no delay to invasive
strategy, there is no preference for either strategy
Fibrinolysis is preferred if:
•
Early presentation (<3 hours from symptom onset and delay
to an invasive strategy)
•
Invasive strategy is not an option
-
Catheterisation laboratory is occupied or not available
-
Vascular access difficulty
-
Lack of access to a skilled PCI laboratory (Individual
operator experience of > 75 primary PCI cases/year or
team experience of > 36 primary PCI cases/ year)
•
Delay to invasive strategy
-
prolonged transport
-
(Door to balloon)-(Door to needle time) more than 1
hour.
-
Medical contact to balloon or door to balloon time more
than 90 minutes.
Kaul et al have emphasised on the early use of fibrinolytic
agents and antiplatelet drugs.
Recent Advances in the Management
of AMI
An invasive strategy is preferred if:
•
Skilled PCI laboratory is available with surgical back up.
•
High risk STEMI
-
Cardiogenic shock
-
Killip class >3
•
Contraindications to fibrinolysis including increased risk
of bleeding and intracranial haemorrhage.
•
Late presentation
-
•
Diagnosis of STEMI is in doubt.
Symptom onset was more than 1 hour ago.
Haemodynamically unstable patients, patients in cardiogenic
shock and rarely those with refractory ischaemia, may require
additional support with intraaortic balloon counter pulsation
(IABP). IABP reduces preload and increases coronary perfusion
in diastole. Percutaneous left ventricular assist devices may
also allow time for the stunned or hibernating myocardium to
recover.11
Discussing recent advances Mardikar et al have highlighted
the different modalities available, including thrombus aspiration.
The TAPAS trial showed a decline in mortality rate at the end
of 30 days in patients who had undergone aspiration. Newer
antiplatelet agents like prasugel and ticagrelor have also helped
© SUPPLEMENT TO JAPI • december 2011 • VOL. 59
in lowering the restenosis rate. They have drawn attent to the
posibility of stem cells in revascularisation.
Guidelines of Ami Management12
Each geographic locality should have its plan for management
of STEMI patients, including which hospitals should receive
them from the community. Units capable of obtaining a rapid
ECG diagnosis and risk stratifying these patients should
transfer them expeditiously to hospitals with facilities for early
percutaneous coronary intervention. Early pharmacotherapy
including antiplatelet agents, anticoagulant, statin should be
initiated in the receiving hospital. In this issue Iyengar and
Godbole have stated that even with PAMI being practised
more frequently thrombolysis still has a part to play in early
revascularistion, especially with the ready availability of newer
antithrombolytics like tenectaplase. However, they also stress
that TIMI 3 flow may not be achieved always and that PAMI
may have to be taken recourse to. Banerjee and Kumar have
emphasised the early and late modalities of management.
Management of Complications in AMI
Complications in AMI may be electrical (tachy or brady
arrhythmias) or mechanical. It is important to recognise these
early to ensure survival and recovery of the patient with AMI.
Cardiogenic shock may result from right ventricular infarction,
free wall rupture, ventricular septal rupture, papillary muscle
rupture or pump failure resulting from infarction of a large
territory of myocardium.
Early echocardiography can help in identifying and
differentiating the causes of mechanical failure.Five therapeutic
modalities are used to treat patients in Cardiogenic shock
which include vasopressors, mechanical support with IABP or
ventricular assist devices, fibrinolysis, PCI and CABG. The first
two treatment modalities are useful but temporary modalities.
Revascularisation is associated with an improvement in survival.
The SHOCK trial13 evaluated the outcome in patients with AMI in
Cardiogenic shock. 86% patients received IABP and two groups
were randomised to early revascularisation with PCI or CABG
or to initial medical stabilisation. The mortality was lower and
long term survival was better in the group randomised to early
revascularisation.
Free wall rupture, ventricular septal rupture and papillary
muscle rupture require early operative intervention after early
stabilisation with IABP. Surgical survival is determined by early
surgery, short duration of Cardiogenic shock and milder degree
of systolic biventricular impairment.14
First degree and second degree Type I blocks do not affect
survival and do not require invasive therapy with pacing.
However if the ventricular rate falls below 50 beats/min and
the patient is symptomatic treatment with atropine is indicated.
Transvenous pacing is almost never required in this situation.
Complete AV block can occur in patients with anterior and
inferior infarction. In patients with anterior infarction complete
heart block can result suddenly after 12-24 hours and occurs
due to extensive septal necrosis which involves the bundle
branches. The prognosis is poor in this group of patients even
after pacing because of the extensive myocardial necrosis which
has occurred. In this issue Mullasari et al have dealt extensively
with the complications arising from infarctions. Cardiac failure
and arrhythmias are commonly seen though complications
like myocardial rupture and aneurysm formation are relatively
uncommon. Heart blocks are quite common and often transitory.
© SUPPLEMENT TO JAPI • december 2011 • VOL. 59 Future of Thrombolytic Therapy-An
Indian Perspective
An estimated 31.8 million in India have coronary heart disease
(CHD).15 This translates into 11% prevalence in urban India.
However, hospitals with PCI capabilities may not be available to
all, especially in rural areas and smaller cities. If patients present
to the community hospitals (which have no facilities for PCI) in
these areas within 12 hours of onset of infarction (LATE trial17),
thrombolysis is an option that may be used. The data from 22
trials of fibrinolytic therapy was pooled and it was seen that the
earlier the treatment was started after the onset of symptoms,
the greater was the benefit. The benefit decreased in a non linear
fashion with incremental delays in time to thrombolysis after
onset of symptoms. The greatest benefit was in the first hour after
the onset of symtoms16 (the Golden Hour). Also one must keep
in mind that many of the patients may not be affording PCI and
majority are not insured. In this scenario, thrombolysis if given
within the Golden hour may prove to be not only life saving
but also a cost effective approach to treat AMI in our country.
Cardiac Rehabilitation after MI
The effect of exercise training after MI is to improve exercise
capacity and quality of life. Exercise training helps in decreasing
the myocardial oxygen demand and also helps in improving
the endothelial function.18 All patients after acute MI should be
encouraged to enrol for a physician supervised rehabilitation
program. Many hospitals have started offering this rehabilitation
as a package included with the PCI, where patients do not
have to bear any additional cost. However if approved and
reimbursed by insurance companies, then it will see a greater
rise in utilisation by patients. In this issue Contractor has dealt
extensively on the process of early and late rehabilitation.
References
1. Yusuf S,Vaz M, Pais P: Tackling the challenge of disease burden in
developing countries. Am Heart J 148;1:2004.
2. Luepker RV, Apple FS, Christenson RH, et al:case definitions
for acute coronary disease in epidemiology and clinical research
studies. Circulation 2003;108:2543.
3. Alpert JS, Thygesen K, Antman E, et al: Myocardial infarction
redefined: A consensus document of the joint European society of
Cardiology /American College of Cardiology Committee for the
redefinition of myocardial infarction. J Am Coll Cardiol 36;959:2000.
4. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group.
Indications for fibrinolytic therapy in suspected acute myocardial
infarction: collaborative overview of early mortality and major
morbidity results from all randomised trials of more than 1000
patients. Lancet 1994;343:311–322.
5. Boersma E, Maas AC, Deckers JW, Simoons ML. Early thrombolytic
treatment in acute myocardial infarction: reappraisal of the golden
hour.Lancet 1996;348:771–775.
7
6. Morrison LJ, Verbeek PR, McDonald AC, Sawadsky BV, Cook
DJ. Mortality and prehospital thrombolysis for acute myocardial
infarction: a meta-analysis. JAMA 2000;283:2686–2692.
7. Pre-hospital thrombolysis delivered by paramedics is associated
with reduced time delay and mortality in ambulance-transported
real-life patients with ST-elevation myocardial infarction. Erik
Bjorklund, Ulf Stenestrand, Johan Lindback, Leif Svensson, Lars
Wallentin, and Bertil Lindahl. European Heart Journal 2006;27:1146–
1152.
8. Impact of Prehospital Thrombolysis for Acute Myocardial Infarction
on 1-Year Outcome: Results From the French Nationwide USIC
2000 RegistryNicolas Danchin, Didier Blanchard, Philippe Gabriel
Steg, Patrick Sauval, GuyHanania, Patrick Goldstein, Jean-Pierre
Cambou, Pascal Guéret, Laurent Vaur, Youcef Boutalbi, Nathalie
Genès and Jean-Marc Lablanche. Circulation 2004;110:1909-1915.
9. Anderson JL, Adams CD, Antman EM, et al: ACC/HA 2007
guidelines for the management of patient with unstable angina/
non ST elevation myocardial infarction. Circulation 2007;116:e148.
10. Antman EM, Anbe DT, Armstrong PW:ACC/AHA guidelines for the
management of patients with ST-elevation myocardial infarction:
A report of the American College of Cardiology/ American Heart
Association Task force on practice guidelines. (Commitee to revise
the 1999 guidelines for the management of patients with acute
myocardial infarction). Circulation 2004;110:e82.
11. Thiele H, Smalling RW,Schuler GC: Percutaneous left ventricular
assist devices in acute myocardial infarction complicated by
cardiogenic shock. Eur Heart J 2007;28:2057.
12. ACC/AHA/SCAI Guidelines on Percutaneous Coronary
Intervention (updating the 2005 Guideline and 2007 focused
Update): a report of the American college of Cardiology
Foundation/American Heart Association Task Force on Practice
Guidelines. Circulation 2009;120:2271.
13. Hochman JS, Sleeper LA, Webb JG: Early revascularisation and long
term survival in Cardiogenic shock complicating acute myocardial
infarction. JAMA 2006;295:2511.
14. Poulsen SH, Praestholm M, Munk K: Ventricular septal rupture
complicating acute myocardial infarction: Clinical characteristics
and contemporary outcome. Ann Thorac Surg 2008;85:1591.
15. Gupta R: Burden of coronary heart disease in India. Ind Heart J
2005;57:632.
16. Boersma E, Maas AC, Deckers JW : Early thrombolytic treatment in
acute myocardial infarction: Reappraisal of the golden hour. Lancet
1996;348:771.
17. A randomized trial of late reperfusion therapy for acute myocardial
infarction. Thrombolysis and Angioplasty in Myocardial
Infarction-6 Study Group EJ Topol, RM Califf, M Vandormael, CL
Grines, BS George, ML Sanz, T Wall, M O’Brien, M Schwaiger and
FV Aguirre. Circulation 1992;85:2090-2099.
18. Hambrecht R, Wolf A, Glen S: Effect of exercise on coronary
endothelial function in patients with coronary artery disease. N
Eng J Med 2000;342:454.