INTERVENTIONS
IN ACUTE CORONARY SYNDROME - IS IT SERVING ITS PURPOSE ?
Rajesh Rajani
Consultant Cardiologist, PD Hinduja National Hospital and Medical Research Centre.
Acute myocardial infarction results from
total occlusion of coronary arteries i.e. the arteries supplying the heart muscle.
The treatment for this condition is early and total opening of the occluded
artery so as to prevent or reduce death of myocytes, namely the heart muscle.
This used to be achieved in earlier times using drugs which dilate the coronary
arteries and thereafter by drugs which make the blood thin and facilitates the
flow through narrowed arteries (amyl nitrate, nitroglycerine, sorbitrate, heparin,
etc.). It was found on pathological examination of coronary arteries in patients
dying of heart attack that the majority of them had occlusion of the arteries
due to clot or thrombus. Many researches went into improving the status of patients
with acute myocardial infarction based on the above findings and this led to
development of better drugs for dissolving the blood clot viz. streptokinase,
tissue plasminogen activator, etc. The so called ‘Clot Busters’. Inspite of
all this, the mortality rate in patients suffering from acute myocardial infarction
used to be high and it was felt that something was being missed. By the time
coronary angiography has been perfected, pathogenesis of the atherosclerotic
plaque and its subsequent rupture and fissuring leading to release of many endogenous
substances which initiate thrombosis was understood in greater details.
In 1977, Dr Andreas Gruentizig did the first coronary angioplasty in a critically
narrowed coronary artery with successful results. During this time it was thought
that angiography in acute myocardial infarction was not safe and should be avoided.
[1] However experience in the last 15 years has shown that
angiography in acute myocardial infarction is safe and reliable. [2]
Angiography studies done during acute myocardial infarction showed that incidence
of total occlusion of the major coronary arteries is around 40% in the infarct
related vessel. [3] Thrombotic occlusion was seen as the major
cause in most of the patients and early reperfusion either using pharmacologic
means or mechanically using angioplasty would be the ultimate aim in the treatment
of acute myocardial infarction. Early perfusion was established by Dr. Geoffrey
Hartzler in patients with acute myocardial infarction using Gruentzig’s technique
of angioplasty. He published his data in 41 patients in 1983. He proceeded with
angioplasty without resorting to thrombolysis. The results showed that the procedure
was safe and had a high success rate. The left ventricular function had shown
dramatic improvement on left ventriculography. [4] In seven
years 2073 cases were done and the results were encouraging. Mortality averaged
8.3% and was lowest in the single vessel group and highest in patients with
cardiogenic shock. Although patients with cardiogenic shock had highest mortality,
they were the ones who benefited the most. Emergency CABG was required in 4.9%
of patients. About 4.5% of the patients had recurrent ischaemic events or had
non-fatal infarction. [5] Over the years the success rate in
primary angioplasty had non-fatal infarction. [5] Over the
years the success rate in primary angioplasty increased to 96% and mortality
rates reduced. [6-9] Due to the pioneering efforts of O’Keefe,
Grines, Brodie, Stone, Khan, Zijlstra,Rentrop,
O’Niell, Himbert and DeWood the technique of primary angioplasty was accepted
as the first line therapy for acute myocardial infarction and for impending
infarction - unstable angina. [ 3, 7,10-17
]
The next issue to be settled was : Is primary angioplasty superior to thrombolytic
therapy for acute myocardial infarction? The issue was settled in a multicentre
trial in which primary angioplasty was compared to t-PA therapy for acute myocardial
infarction. The results showed that immediate angioplasty or primary angioplasty
reduced the combined occurrence of nonfatal reinfarction of death, lower rate
of intracranial bleed and similar left ventricular function.[14]
This trial enrolled 395 patients presenting within 12 hours of onset of myocardial
infarction. 195 underwent angioplasty and 200 received t-PA followed by conservative
care. Among the angioplasty group 90% of the patients underwent the procedure
and the success rate was 97%. No patient went for CABG. In-hospital mortality
in angioplasty group was 2.6% which was far lower than 6.5% in the t-PA group.
Reinfarction or death occurred in 5.1% of angioplasty patients as compared to
12.5% of the t-PA group. By six months 8.5% of the angioplasty patients had
reinfarction or death as compared to 16.8% of the t-PA group. [14]
The CORAMI study group in 1993 published their data that in 20% - 50% of the
patients depending on the agent used for thrombolysis, there is failure to achieve
early reperfusion of the infarct - related artery. These "thrombolysis
failures" carry a substantially increased risk of early and late death
compared with patients who have a patent infarct - related artery within 90
minutes of thrombolysis. Angiography done in such cases emerged as the treatment
modality for "thrombolysis failures" and was called as "rescue
angioplasty". In a study of 299 patients of acute myocardial infarction
treated with thrombolysis within 6 hours of onset of symptoms and angiography
at 90 minutes after the start of thrombolysis it was clearly shown that thrombolysis
failed in 29.5% of patients, defined as TIMI-0 or 1 flow (sluggish antegrade
flow) in the infarct related artery. The actual number of thrombolysis failure
was 87/299 and out of these 72 underwent and emergent or rescue angioplasty
within 8 hours of onset of symptoms, rest of the patients were excluded as the
coronary artery anatomy was found unsuitable for angioplasty. Success was defined
as TIMI 3 or > flow in the infarct related artery with residual stenosis
of < 40%. Rescue PTCA was successful in 90% (65/72) patients. Predischarge
angiography was done in 88% of patients at an average of 8.3 days and it showed
TIMI 3 flow in infarct related artery with residual stenosis < 50% in 93%
of cases. Two patients had symptomatic reocclusion and one had asymptomatic
reocclusion. Overall reocclusion rate was 7%. Long term (16 æ 12 months)
follow up was available in 94% patients, 74% were asymptomatic and 88% were
event free survivors. [18] various large trials including
CORAMI, RESCUE and others assessed the effectiveness of rescue angioplasty.
Technical success is lower than that of direct or primary angioplasty indicating
that patients who fail to respond to thrombolysis are in general a more difficult
subset for angioplasty. The likelihood of complications such as ruptured plaque
and bleeding complications are also more frequent in them. These patients have
higher mortality in the range of 10-17% as compared to the primary angioplasty
group. However, despite these shortcomings, the advantage of improved LV function,
reduced incidence of heart failure and reduced mortality at 1 month and subsequently,
favours this procedure immensely.
The 10-15% incidence of recurrent ischaemia and reocclusion following angioplasty
in patient with acute myocardial infarction used to make one feel insecure about
the outcome in a given patient, but with the introduction of stents and their
utilisation in this setting the procedure has become more acceptable and safe.
Incidence of recurrent ischaemia and reocclusion has further reduced but theincidence
of slow flow following these procedures used to be a cause for concern. Introduction
of glyocprotein IIb IIIa inhibitors e.g. Abxicimab, Ticlopidine and clopidogrel
has reduced the incidence of this complication too.
In conclusion the preferred modality
of acute coronary syndromes in the next millennium would be angioplasty with
or without addition of newer devices and pharmacological agents.
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