The presence of sudden chest pain that lasts more than 30 minutes especially in a patient with multiple risk factors. The pain is deep and visceral; adjectives commonly used to describe it are heavy, squeezing, and crushing, although occasionally it is described as stabbing or burning. It is often accompanied by weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom.
Although pain is the most common presenting complaint, it is by no means always present. The proportion of painless AMIs is greater in patients with diabetes mellitus, and it increases with age. In the elderly, AMI may present as sudden-onset breathlessness, which may progress to pulmonary edema.
The combination of substernal chest pain persisting for >30 min and diaphoresis strongly suggests AMI.
Myocardial infarction (MI) progresses through the following temporal stages: (1) acute (first few hours to 7 days), (2) healing (7 to 28 days, and (3) healed (29 days and beyond). When evaluating the results of diagnostic tests forAMI, the temporal phase of the infarction process must be considered.
Diagnosed by the presence of at least 2 of the following:
- History of prolonged chest pain or anginal equivalent.
- ECG changes consistent with ischemia or necrosis.
- Elevated cardiac enzymes.
The laboratory tests of value in confirming the diagnosis may be divided into 4 groups: (1) electrocardiogram (ECG), (2) serum cardiac markers, (3) cardiac imaging, and (4) nonspecific indexes of tissue necrosis and inflammation.
During the initial stage of the acute phase of MI, total occlusion of the infarct artery produces ST-segment elevation. Most patients initially presenting with ST-segment elevation evolve Q waves on theECG and are ultimately diagnosed as having sustained a Q-wave MI. A small proportion may sustain only a non-Q-wave MI. When the obstructing thrombus is not totally occlusive, obstruction is transient, or if a rich collateral network is present, no ST-segment elevation is seen. Such patients are initially considered to be experiencing either unstable anigna or a non-ST-segment elevation MI (NSTEMI). Among patients presenting without ST-segment elevation, if a serum cardiac marker is detected and no Q wave develops, the diagnosis of non-Q-wave MI is ultimately made. A minority of patients who present initially without ST-segment elevation may develop a Q-wave MI. Previously it was believed that transmural MI is present if the ECG demonstrates Q waves or loss of R waves, and nontransmural MI may be present if the ECG shows only transient ST-segment and T-wave changes. However, electrocardiographic-pathologic correlations are far from perfect; and therefore a more rational nomenclature for designating electrocardiographic infarction is now commonly in use, with the terms Q-wave and non-Q-wave MI replacing the terms transmural and nontransmural MI, respectively.
Certain proteins, called serum cardiac markers, are released into the blood in large quantities from necrotic heart muscle after AMI. The rate of liberation of specific proteins differs depending on their intracellular location and molecular weight, and the local blood and lymphatic flow.
The temporal pattern of protein release is of diagnostic importance, but contemporary urgent reperfusion strategies necessitate making a decision (based largely on a combination of clinical and ECG findings) before the results of blood tests have returned from the central laboratory. Rapid whole-blood bedside assays for serum cardiac markers are now available and may facilitate management decisions, particularly in patients with nondiagnostic ECGs.
- CKMB: The MB isoenzyme of creatine phosphokinase is more specific to AMI than CK. However, it may still be elevated in skeletal muscle injury. Rather than attempting to make the diagnosis ofAMI on the basis of a single measurement of CK and CKMB, clinicians should evaluate a series of measurements obtained over the first 24 h. Skeletal muscle release of CKMB typically produces a "plateau" pattern, whereas AMI produces a CKMB elevation that peaks approximately 20 h after the onset of coronary occlusion. When released into the circulation, the myocardial form of CKMB (CKMB2) is acted on by the enzyme carboxypeptidase, which cleaves a lysine residue from the carboxyl terminus to produce an isoform (CKMB1) with a different electrophoretic mobility. A CKMB2:CKMB1 ratio of>1.5 is highly sensitive for the diagnosis of AMI, particularly 4 to 6 h after the onset of coronary occlusion.
- The MB-CK fraction appears in 4 hours after onset of infarction and peaks at about 24hrs with a duration of 72 hours.
- CK MB: 4h - 24h - 72h
- Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) have amino acid sequences different from those of the skeletal muscle forms of these proteins. These differences have permitted the development of quantitative assays for cTnT and cTnI with highly specific monoclonal antibodies. Since cTnT and cTnI are not normally detectable in the blood of healthy individuals but may increase afterAMI to levels over 20 times higher than the cutoff value (usually set only slightly above the noise level of the assay), the measurement of cTnT or cTnI is of considerable diagnostic usefulness, and they are now the preferred biochemical markers for MI. The cardiac troponins are particularly valuable when there is clinical suspicion of either skeletal muscle injury or a small MI that may be below the detection limit for CK and CKMB measurements. Levels of cTnI may remain elevated for 7 to 10 days after AMI, and cTnT levels may remain elevated for up to 10 to 14 days. Thus, measurement of cTnT or cTnI has replaced measurement of lactate dehydrogenase (LDH) and its isoenzymes in patients with suspected MI who come to medical attention more than 24 to 48 h after the onset of symptoms.
- LDH on the other hand appears 12 hours after the infarct and peaks 2 days later to last 14 days. LDH has been largely replaced with the more specific cardiac troponin for patients with suspected AMI presenting after the initial 48 hours have passed.
- LDH: 12h - 48h - 14 days
- CK: Creatine phosphkinase has been replaced by CKMB due to lack of specificity of CK in AMI.
- SGOT, SGPT
Two-dimensional echocardiography is the most frequently employed imaging modality in patients with AMI. Abnormalities of wall motion are almost universally present.
Several radionuclide imaging techniques are available for evaluating patients with suspected AMI. However, these imaging modalities are used less often than echocardiography because they are more cumbersome and they lack sensitivity and specificity in many clinical circumstances. Myocardial perfusion imaging with 201Tl or 99mTc-sestamibi, which are distributed in proportion to myocardial blood flow and concentrated by viable myocardium reveal a defect ("cold spot") in most patients during the first few hours after development of a transmural infarct. However, although perfusion scanning is extremely sensitive, it cannot distinguish acute infarcts from chronic scars and thus is not specific for the diagnosis of acute MI.
Management of MI
Recognize patients that are candidates for reperfusion therapy. Patients presenting with new ST elevation or presumed new LBBB is indicative of transmural infarction and are indicated for thrombolytic therapy within 30mints of admission or 1ry PTCA within 60mints of arrival to hospital.
Initial treatment for all patients with chest pain and suspected myocardial infarction ( whether or not they are indicated for reperfusion therapy they should all receive the following):
- Sublingual nitroglycerin 0.4mg q 5mints should be administered to all patients in the absence of hypotension or marked tachycardia or inferior infarction complicated by right ventricular infarction.
- Analgesics: very important as it reduces the circulating catecholamines and myocardial oxygen consumption. Morphine sulfate is choice and given only if symptoms persist after 0.4mg sublingual nitroglycerin q 5mints.
- Antiplatelets: 165-325mg PO reduces mortality from myocardial infarction.
- Anticoagulation: as in ischemia.
- Beta-antagonists: reduce myocardial ischemia and may limit infarct size. Therapy is initiated with IV metoprolol 5mg. Can be repeated q5mints till total 15mg (loading). Patients tolerating the loading dose are switched to oral 50mg q6-12hrs then 100 mg PO bid (/ atenolol 100mg qd). Contraindications to beta blockers are:
- Rales over > 1/3 of lung fields.
- HR < 60/mint
- Sys BP <90.
- PR >250msec
- advanced heart block.
- bronchospastic lung disease.
- severe PVD.
- IV fluids for those in shock
- ACE-inhibitors in all normotensive patients especially if there is clinical evidence of heart failure.
- Oxygen: arterial O2 is obtained at admission only if the patient is in respiratory distress and is not a candidate for thrombolytic therapy. 2-4 L/mint via nasal cannulation. If patients do not have hypoxemia they can be discontinued after 6hrs. increasing O2 to supranormal levels is not indicated as this increases the BP and resistance.
Patients should be stratified into those that are candidates for thrombolytic therapy and those that are candidates for angiography and PTCA. Thrombolytic therapy is the first choice for restoring coronary perfusion in patients with acute MI, assuming the absence of contraindications for its use.
Patients in need of thrombolytic therapy:
- All patients presenting within 12hrs of a prolonged ischemic attack (>30mints that is associated with new? ST segment elevation of at least 0.1 mV (>1 mm) in at least two contiguous leads).
- Patients with marked ST segment depression (>2 mm) in the anterior leads that is indicative of posterior wall infarction and
- Patients with prolonged chest pain and presumed new LBBB.
Fibrinolytic agents will induce clot lysis in 60-90% of patients and will normalize coronary blood flow in 30-40% of infarct-related arteries by 90 minutes, depending on the agent used.
Absolute Contraindications to Fibrinolytic Therapy
- Active internal bleeding
- CNS neoplasm, AV malformation, or aneurysm.
- CNS procedure or CVA within two months.
- Severe uncontrolled hypertension (over 200/130 or complicated by retinovascular disease or encephalopathy)
- Known bleeding diathesis
- MI due to aortic dissection
- Allergy to either streptokinase or anistreplase, if streptokinase or anistreplase will be used
Relative Contraindications to thrombolytic therapy
- Age over 75
- Cerebrovascular disease
- Pregnancy or early postpartum
- Recent major surgery (less than 10 days), noncompressable vessel puncture, or organ biopsy
- Recent trauma, including CPR of over 2 minutes duration
- Recent GI bleeding or active ulcer disease (less than 10 days)
- Acute pericarditis or subacute bacterial endocarditis
- Septic thrombophlebitis
- High likelihood of left heart thrombus (eg. mitral stenosis with atrial fibrillation)
- Known coagulation defects, including anticoagulant therapy
- Significant liver dysfunction
- Conditions associated with bleeding risks, such as diabetic retinopathy.
- Terminal cancer or other end-stage disease
- Recent streptococcal infection, if streptokinase or anistreplase will be used
Adjuncts to thrombolysis:
Antithrombotic therapy in the form of anti-patelets and anti-thrombotics in addition to beta adrenergic blockers.
Those in need of emergency angiography and possible PTCA are: (within 60mints of admission)
- Patients with chest pain and persistent ST elevation who present more than 12 hours after the onset of acute MI,
- Patients with persistent ST depression,
- Patients with refractory angina symptoms and nondiagnostic ECG changes.
- Patients with contraindications to thrombolysis usually are candidates for primary PTCA.
Those in need of emergency CABG:
Emergency CABG is indicated in patients with refractory ischemia or cardiogenic shock whose coronary anatomy is not suitable for PTCA, in patients in whom PTCA has failed, and in patients with mechanical complications of MI. Insertion of an intra-aortic balloon pump usually is indicated to stabilize these patients before the surgical procedure.
Risk stratification & subsequent management of MI:
This is done by clinical assessment and echocardiography at 24 hours.
High risk patients (patients with any of the following):
- Heart failure, heart block
- Previous myocardial infarction
- Recurrent myocardial infarction or angina during the 24 hours.
These should remain hospitalized for several days after stabilization and undergo a coronary angiography to determine if in need of PTCA/ CABG.
2. Low risk patients (those without any of the above criteria).
These patients can be transferred to a monitored telemetry floor after 24-36 hours. If ambulatory without recurrent ischemia they can be discharged within 4 days and undergo subsequent symptom limited stress testing as outpatients within 10 -14 days. Those with induceable ischemia are subsequently sheduled for PTCA / CABG. If stress testing goes well then another one is usually performed at 6-8 weeks before going to work.
After all the above is accomplished patients are put on a diet and exercise program to reduce co-existing risk factors e.g. lipid lowering drugs in hypercholestrolemia, estrogens in postmenopausal patients.
- Coexisting medical conditions are treated appropriately.
- Antiplatelets (Aspirin 75-325mg) given daily indefinitely (reduces vascular events by 30%).
- Warfarin for 6 months if large anterior infarct, aneurysm or mural thrombus. It is given for life if co-existing atrial fibrillation and severe left ventricular failure.
- Beta blockers are given indefinitely unless contraindicated or very low risk group and young (reduces mortality from all causes by 25%).
- Calcium channel blockers are given if beta blockers are contraindicated.
- Angiotensin converting enzyme (ACE) inhibitors are given to all patients for the first 6 weeks. It is given indefinitely if left ventricular failure or if the ejection fraction is less than 40% (decreases 2 year mortality by 30%).
- Nitrates in symptomatic ischemia or heart failure.
33% of patients will die from their 1st myocardial infarction.