Acute myocardial infarction

Published on 02/04/2015 by admin

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14 Acute myocardial infarction

Instruction

This patient has had a myocardial infarction 2 days ago; would you like to take a short history and examine him?

Salient features

Examination

• Hands: nicotine staining of fingers

• Pulse: check pulse rate (keeping in mind heart block and tachycardia), rhythm (keeping in mind atrial fibrillation, ventricular arrhythmias)

• Check blood pressure

• JVP may be raised in cardiac failure or right ventricular infarction

• Eyes: look for arcus senilis, xanthelasma

• Cardiac apex: look for double apical impulse (ventricular aneurysm)

• Auscultate for fourth heart sound, pericardial rub, pansystolic murmur of papillary muscle dysfunction (or ventricular septal defect)

• Examine:

• chest for crackles and pleural effusion

• abdomen for tender liver of cardiac failure

• legs for deep venous thrombosis and peripheral pulses.

• Tell the examiner that you would like to:

• check the ECG for ST segment changes (Fig. 14.1)

• know whether serum cardiac markers were elevated (be prepared to compute the TIMI (thrombolysis in myocardial infarction) risk score if asked, see below).

Fig. 14.1 Principal electrocardiographic indicators of acute infarction.

Diagnosis

This patient with myocardial infaction (aetiology) has papillary muscle dysfunction (lesion) and is in Killip class II cardiac failure (functional status).

Be prepared to discuss the ‘number needed to treat’ (NNT) for each therapy:

Table 14.1: NNT† to treat in acute MI.

Questions

Mention some causes of elevated troponin not the result of acute coronary syndrome

• Myocarditis

• Heart failure

• Thromboembolism.

Describe the Killip (or Killip–Kimball) classification

The Killip classification is used to characterize heart failure following MI (Am J Cardiol 1967;20:457–64):

Killip I: absent third heart sound and absence of crackles

Killip II: third heart sound or crackles in <50% of lung fields

Killip III: crackles in greater than 50% of lung fields

Killip IV: cardiogenic shock.

What are the three main types of acute coronary syndrome

• Unstable angina

• Non ST elevation MI (NSTEMI)

• ST elevation MI (STEMI).

How would you use the ECG to localize STEMI?

• Anterior or anteroseptal: The QS complexes in leads V₁ and V₂ indicate anteroseptal infarction. A characteristic notching of the QS complex, often seen with infarcts, is present in lead V₂. The septum is supplied with blood by the left anterior descending coronary artery. Septal infarction generally suggests this artery or one of its branches is occluded, whereas a strictly anterior infarct generally results from occlusion of the left anterior descending coronary artery.

• Anterolateral: ST segment elevation in leads I, L, and V₁ to V₆ with Q waves in V₁ to V₄. (Fig. 14.1B,C)

• Posterior: tall R waves in leads V₁ and V₂. In most cases of posterior infarctions, the infarct extends either to the lateral wall of the LV (resulting in characteristic changes in lead V₆) or to the inferior wall of that ventricle (resulting in characteristic changes in leads II, III and aVF). Because of the overlap between inferior and posterior infarctions, the more general term inferoposterior is used when the ECG shows changes consistent with either inferior or posterior infarction.

• Inferior: ST elevations in leads II, III, and aVF and the reciprocal ST depressions in leads I and aVL. Inferior wall infarction is generally caused by occlusion of the right coronary artery. Less commonly, it occurs because of a left circumflex coronary obstruction.

• Right ventricular infarction: Q waves and ST segment elevations in leads II, III and aVF are accompanied by ST elevations in the right precordial leads.

This classification is not absolute, and infarct types often overlap.

How would you manage a patient with acute MI?

• In A&E, a patient with chest pain should have a quick clinical examination and an ECG done within 10 min of arrival to hospital.

• Aspirin: chewable non-coated 160–325 mg should be administered immediately and then 160–325 mg daily. In the ISIS-2 and ISIS-3 trials, 160 mg dosage was effective whereas a 325 mg dose was used successfully in GISSI-2. An initial large dose of aspirin of 325 mg orally or 160 mg chewable aspirin is preferred because lower doses may still allow significant thromboxane activity and may take a few days.

• Pain relief: immediate relief of pain should be a top priority because severe pain can result in autonomic disturbances that can result in sudden death.

• Reperfusion strategies: either thrombolysis or primary PTCA should be performed within 30 min of the patient’s arrival in hospital.

• Beta-blockers: patient should receive beta-blockers when there are no contraindications within 12 h of onset of infarction, irrespective of administration of concomitant thrombolytic therapy or performance of primary angioplasty.

• ACE inhibitors: should be administered within the first 24 h of a suspected acute STEMI in ≥2 anterior precordial leads or with clinical heart failure in the absence of hypotension (systolic BP <100 mmHg) and known contraindications to use of ACE inhibitors.

What is a silent myocardial infarct?

A painless infarct, common in diabetics and the elderly (particulary women); it may present with complications of myocardial infarction.

How is short-term risk determined in acute coronary syndromes?

The TIMI risk score can be used for unstable angina/NSTEMI and for STEMI.

Unstable angina/NSTEMI

The TIMI risk score for NSTEMI is one method of evaluating short-term (14-day) risk for death and non-fatal MI in patients presenting with unstable angina and NSTEMI. The TIMI trial risk score for death or myocardial infarction at 14 days assigns a value of 0 when a factor is absent and 1 when a factor is present. The score utilizes seven independent risk factors:

• Age >65 years

• >3 risk factors for coronary artery disease

• Documented coronary artery disease at catheterization

• ST deviation >0.5 mm

• >2 episodes of angina in last 24 h

• Aspirin within prior 7 days

• Elevated cardiac markers.

Use of this scoring system was able to risk-stratify patients across a 10-fold gradient of risk, from 4.7% to 40.9% (p <0.001). The TIMI risk score predicts outcome and response to therapy.

Outcome:

0–2: low risk (8% rate of recurrent MI or death)

3–4: intermediate risk

6–7: high risk (~31% rate of recurrent MI or death).

Response to therapy: patients with higher TIMI risk scores had significant reductions in events when treated with enoxaparin than when treated with unfractionated heparin, treated with a glycoprotein IIb/IIIa antagonist inhibitor compared with placebo, and with invasive compared with conservative strategy.

STEMI

In the TIMI scoring system for STEMI (1 through 14 points), risk rises progressively with higher scores and is maximal for a composite score >8. A score >6 identifies a segment of the population (12%) that has double the mean 30-day mortality risk of the total population. However, this scoring system should not substitute for clinical judgment in individual cases. For example, patients with inferior STEMI, who might be considered to have a low risk of mortality (and for whom many physicians have questioned the benefits of thrombolysis), might actually be in a much higher mortality risk subgroup if their inferior infarction is associated with ST segment elevation in the lateral precordial leads indicating right ventricular infarction, or precordial ST segment depression.

The Global Registry for Acute Coronary Events (GRACE) system

This is another risk score for prediction of death and myocardial infarction that incorporates renal dysfunction.

What are TIMI grades?

Grades (0–3) determined in the thrombolysis in myocardial infarction trial (TIMI) measure coronary blood flow and luminal narrowing:

0: no flow of contrast beyond the point of occlusion

1: penetration with minimal perfusion (contrast fails to opacify the entire coronary bed distal to the stenosis for the duration of investigation)

2: partial perfusion (contrast opacifies the entire distal coronary artery, but the rate of entry or clearance or both is slower in the previously blocked artery than in nearby normally perfused vessels

3: complete perfusion (contrast filling and clearance are as rapid in the previously blocked vessel as in normally perfused vessels).

Which thrombolytic agents are available?

• Streptokinase: for non-anterior MI

• Tenecteplase: for anterior MI, previous streptokinase use, systolic BP <100 mmHg, new left bundle branch block; can be given by paramedics and administered as a bolus

• Alteplase (rt-PA): in younger patients with anterior MI; given within 6 h of symptoms in accelerated manner and followed by heparin

• Reteplase: given in two intravenous boluses 2 h apart.

What is the relation between thrombolysis and onset of symptoms?

Thrombolytic therapy reduces mortality and limits infarct size. The shorter the interval between the onset of symptoms and the initiation of thrombolysis, the greater is the survival. The greatest benefit occurs if the treatment is initiated within the first 3 h, when a 50% or greater reduction in mortality rate can be achieved. The magnitude of benefit declines rapidly thereafter, but a 10% mortality reduction can be achieved up to 12 h after the onset of pain.

Duration from symptom onset to therapy initiation	Lives saved per 1000 treated
<60 min	65
2–3 h	27
4–6 h	25
7–12 h	8

What is the benefit of late administration of thrombolytic therapy?

ISIS-2 (Lancet 1988;ii:349–60) showed benefit for up to 24 h (after onset of symptoms) with thrombolysis, but more recent studies—the LATE (Late Assessment of Thrombolytic Therapy) and EMERAS (Estudio Multicentrico Estreptoquinasa Republicas de America del Sur)—have shown no benefit for treatment given beyond 12 h.

What is the role of heparin with thrombolysis?

In the ISIS-3 (Lancet 1992;339:753–70) and GISSI-2 (Lancet 1990;336:65–75) studies, heparin therapy was not beneficial with streptokinase or anistreplase, and it is believed that it may even be harmful. The GUSTO trial showed that early intravenous heparin with tPA results in a further reduction in the mortality rate compared with that found with a combination of heparin and streptokinase.

What is the role of prehospital thrombolysis?

Two studies—the GREAT (Grampian Region Early Administration of Thrombolysis) and EMIP (European Myocardial Infarction Project)—showed that a single bolus dose of anistreplase reduced the total mortality rate. These results suggest that early thrombolysis has greater benefit, and hence the importance in many hospitals for ‘door to needle time’.

What is the role of primary angioplasty in acute infarction?

• Angioplasty results in both lower mortality rates and reduction in the incidence of recurrent ischaemic events. Also angioplasty is associated with lower enzyme rise, better left ventricular function and less reinfarction. Angioplasty led to shorter hospital stay, fewer re-admissions and lower follow-up costs. However, the major limitation of this approach is the access to both facilities and personnel to carry out the procedure.

• Angioplasty should be considered in patients who have recognized contraindication to thrombolysis (even if this means transferring the patient) or who are considered high risk and present with their infarction to a hospital where angioplasty can be performed. Patients who have received thrombolysis and who seem on clinical grounds (reduction in maximal ST segment elevation by 50% and resolution of chest pain) not to have reperfused at 90 min review should be seriously considered for rescue angioplasty, again even if this means transferring the patient.

• Patients who do not receive reperfusion therapy should be treated immediately with fondaparinux.

Why is the Asian population in Britain susceptible to premature myocardial infarction?

Premature ischaemic heart disease in migrants from the Indian subcontinent is associated with insulin resistance. The site of this defective insulin action has been localized to the skeletal muscle by means of positron emission tomography (PET) (Circulation 1995;92(suppl I):16).

What do you know about right ventricular infarction?

Right ventricular infarction presents with retrosternal chest discomfort, nausea, vomiting and diaphoresis, unlike left ventricular infarction, which presents with dyspnoea. On examination in right ventricular infarction, there is a raised JVP with no evidence of pulmonary congestion; the patient often has a low cardiac output with hypotension. The patient typically presents with ST elevation in the inferior leads (II, III and aVF) and in one or more right-sided lead, particularly V₄R. The cornerstones of therapy include restoration of infarct artery patency, intravascular volume expansion and inotropic support.

What do you know about the open-infarct related coronary artery hypothesis?

This hypothesis holds that early reperfusion of the infarct-related coronary artery results in myocardial salvage, which preserves left ventricular function and is responsible for improved survival. Patients with complete occlusion of the coronary artery (TIMI grade 0) 90 min following thrombolysis had a 30-day mortality of 8.4%, whereas mortality was 4% in patients with TIMI grade 3 flow (complete perfusion).

What is the role of glycoprotein IIb/IIIa antagonists as adjuncts to thrombolytic therapy in acute myocardial infarction?

After thrombolytic therapy for acute MI, full anterograde perfusion (TIMI grade 3 flow) occurs in only 29–54% of patients at 90 min, while reocclusion occurs in at least 12%, with increased morbidity and mortality. Thrombolytic therapy may itself be prothrombotic by releasing clot-bound thrombin, which in turn stimulates platelet activation. Preclinical and early clinical trials have suggested that glycoprotein IIb/IIIa receptor blockers (which prevent fibrinogen binding to platelets) used as adjuncts to thrombolytic therapy may improve early patency and reduce the incidence of reocclusion. Though there are as yet no data showing a reduction in mortality from such use of these blockers, a large randomized trial has recently confirmed the early findings on patency and suggests that adjunct treatment with glycoprotein IIb/IIIa receptor blockers may hold promise for better management of acute MI—the results from the GUSTO-AMI phase III trial using abciximab with reduced dose reteplase are awaited.

What are the indications for drug-eluting stents?

According to NICE guidelines (issued in Oct 2003) drug-eluting stent should be used if the person has symptoms of angina and the artery is <3 mm across, or the narrowed part (the ‘lesion’) is >15 mm. When more than one artery is narrowed, the interventional cardiologist should make the decision on which type of stent to use for each artery separately. (Note that the Taxus stent elutes paxlitaxel to inhibit cell division; the Cypher stent elutes sirolimus (previously known as rapamycin), an immunosuppressive agent that reduces inflammation).

What do you know about risk stratification after myocardial infarction?

• Risk stratification before hospital discharge is an important aspect of management and determines whether coronary angiography is indicated. The first step is to determine whether the clinical variables indicating a relatively high risk for future cardiac events are present:

• Patients who have recurrent ischaemia at rest or with mild activity, who have had evidence of congestive heart failure or who are known to have an ejection fraction <40% and in whom there are no contraindications for revascularization should undergo cardiac catheterization and coronary angiography. Revascularization should then be carried out if the coronary anatomy is suitable and there are no contra-indications.

• Patients who have had episode of ventricular fibrillation or sustained ventricular tachycardia >48 h after acute MI should be considered for electrophysiologic study or amiodarone therapy, or both.

• In patients with non-STEMI or unstable angina who appear on clinical grounds to be candidates for coronary revascularization, coronary vascularization should be performed. Revascularization may then be carried out if the coronary anatomy is appropriate.

• Patients without these clinical indicators of high risk should undergo an assessment of left ventricular function (echocardiogram or radionuclide angiogram and submaximal stress) before hospital discharge:

• If the test is negative the patient may return for a symptom limited exercise test at 3 to 6 weeks. If that too is negative they can remain on medical therapy and risk factor reduction.

• If the resting ejection fraction is <40% or if the stress is markedly abnormal (>2 mm ST segment depression, hypotension at peak exercise or low working capacity) then coronary angiography should be carried out if there are no contraindications to revascularization.

• In patients in whom the ECG is not interpretable because of resting ST–T wave abnormalities, digitalis therapy or left bundle branch block, rest and exercise radionuclide myocardial perfusion scintigraphy (with thallium or sestamibi) or rest and exercise echocardiography should be performed. Patients who cannot exercise should undergo pharmacologic stress imaging study such as adenosine or dipyridamole myocardial perfusion scintigraphy or echocardiography with dobutamine or dipyridamole stress. A marked abnormality in any of these tests or a resting ejection fraction <40%, measured by echocardiography or a radionuclide technique, should be followed by coronary angiography.

How is non-invasive testing used to risk stratify patients?

Risk stratification based on non-invasive testing (J Am Coll Cardiol 1999;33:2092–197) comprises:

High risk (>3% annual mortality rate):

• Severe resting LV dysfunction (LV ejection fraction <35%)

• High-risk treadmill score (score ≥−11)

• Severe exercise LV dysfunction (exercise LV ejection fraction <35%)

• Stress-induced large perfusion defect (particularly if anterior)

• Stress-induced multiple perfusion defects of moderate size

• Large, fixed perfusion defect with LV dilation or increased lung uptake (thallium-201)

• Stress-induced moderate perfusion defect with LV dilation or increased lung uptake (thallium-201)

• Echocardiographic wall motion abnormality (involving >2 segments) developing at a low dose of dobutamine (%10 mg/min per kg) or at a low heart rate (<120 beats/min)

• Stress echocardiographic evidence of extensive ischaemia.

Intermediate risk (1–3% annual mortality rate):

• Mild/moderate resting LV dysfunction (LV ejection fraction 35–49%)

• Intermediate-risk treadmill score (−11 to <5)

• Stress-induced moderate perfusion defect without LV dilation or increased lung intake (thallium-201)

• Limited stress echocardiographic ischaemia with a wall motion abnormality only at higher doses of dobutamine involving >2 segments.

Low risk (<1% annual mortality rate):

• Low-risk treadmill score (≥5)

• Normal or small myocardial perfusion defect at rest or with stress

• Normal stress echocardiographic wall motion or no change of limited resting wall motion abnormalities during stress.

What advice would you give this patient on discharge?

Secondary prevention of myocardial infarction (BMJ 1998;316:838–42) as follows:

• Smoking cessation: it should be emphasized to the patient that within 2 years of discontinuing smoking, the risk of a non-fatal recurrent MI falls to the level observed in a patient who has never smoked.

• Lipid profile: a lipid profile should be obtained in all patients with acute MI. Since cholesterol may fall after 24 to 48 h, it is important these measurements be obtained on admission; otherwise a 6-week wait is necessary for cholesterol to reach pre-MI levels. It is desirable to fractionate the cholesterol, and patients with LDL cholesterol >3.37 mmol/l should be treated with lipid lowering agents (p. 616).

• Cardiac rehabilitation: all discharged patients should be referred for outpatient cardiac rehabilitation. Patients should be encouraged to increase activity gradually over 1–2 months.

• Risk factors: diabetes (target HbA1C <6) and hypertension (target BP <130/85 mmHg) should be aggressively controlled.

• Aspirin: led to a 12% reduction in death, a 31% reduction in re-infarction and a 42% reduction in non-fatal stroke in a study of 19791 patients who had myocardial infarctions reviewed by the Antiplatelet Therapy Trialists. Low to medium doses (75–325 mg/day) seems to be as effective as high doses (1200 mg/day).

• Beta-blockers: several controlled trials in >35000 survivors of MI have shown the benefit of long-term treatment with beta-blockers in reducing the incidence of recurrent MI, sudden death and all cause mortality. Beta-blockers reduce myocardial workload and oxygen consumption by reducing the heart rate, BP and contractility, and they increase the threshold for ventricular fibrillation. The beneficial effect of beta-blockers seems to be a class effect, but those with agonist activity do not show a beneficial effect on mortality, and their use cannot be recommended at present.

• ACE inhibitors: low-dose ramipril should be considered in all patients with uncomplicated MI (N Engl J Med 2000;342:145–53). Treatment with full dose ACE inhibitors is recommended for an indefinite period in all patients with congestive heart failure, an ejection fraction <40% or a large regional wall motion abnormality.

Eugene Braunwald (b. 1929) was consecutively Chair and Professor of Medicine in San Diego and Harvard Medical School, Boston. His research interests included heart failure, factors influencing cardiac contraction and hypertrophic cardiomyopathy and he was responsible for the idea that late patency of an occluded artery can lead to clinical benefit. His wife, Nina H Starr Braunwald, was a cardiothoracic surgeon who made important contributions to heart valve replacement.

Thomas Killip described Killips class in 1967.

Professor Jaspal Kooner, is Professor of Clinical Cardiology at Imperial College, Consultant Cardiologist at Hammersmith and Ealing Hospitals. His research includes gene identification of coronary artery disease.

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