Page 2321 - Williams Hematology ( PDFDrive )

2294 Part XII: Hemostasis and Thrombosis Chapter 134: Atherothrombosis: Disease Initiation, Progression, and Treatment 2295

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The criteria for established MI (i.e., event that occurred in the an absolute benefit of 38 vascular events prevented per 1000 patients
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past) is any one of the following: at 1 month with antiplatelet therapy. Aspirin 325 mg/day or a P2Y -
12
receptor antagonist such as clopidogrel is commonly used in the setting
1. Development of new pathologic Q waves on serial ECGs. The patient
may or may not remember previous symptoms. Biochemical mark- of MI. Vorapaxar, a protease-activated receptor-1 (PAR-1) antagonist, is
ers of myocardial necrosis may have normalized, depending on the indicated for the reduction of thrombotic events in patients with a his-
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length of time since the infarct developed. tory of MI or with peripheral artery disease (PAD). Contraindications
2. Pathologic findings of a healed or healing MI. to antiplatelet therapy include active bleeding, coagulopathy, and severe,
untreated hypertension (a relative contraindication). The combination
of dipyridamole and aspirin has not been proven to provide incremental
Clinical Features of Acute Coronary Syndromes clinical benefit over aspirin alone.
Stable angina pectoris is ischemic discomfort symptomatology caused β-Adrenergic Blockade The control of heart rate with β-adrenergic
by a narrowed coronary artery that does not allow sufficient oxygen blocker agents has been efficacious in the setting of acute MI or unstable
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delivery to meet the metabolic demands of the myocardium. Unstable angina. According to guidelines, oral β-blocker should be initiated
angina is defined clinically as a change in the pattern of stable angina to during the first 24 hours of care of STEMI. Intravenous administration
more frequent or more severe symptoms, uninterrupted angina symp- of β-blockers should be given only to selected, hemodynamically stable
toms for 20 minutes or more, or the development of angina at rest. The patients according to guidelines.
term acute coronary syndrome has evolved as a useful description of the Management of Chest Pain A cornerstone of ischemic pain
spectrum of patients presenting with angina pectoris caused by unsta- management has been intravenous nitroglycerin (beginning at 5 to
ble angina through MI. The underlying pathologic mechanism for 10 mcg/min) in combination with morphine sulfate if necessary. Nitro-
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the development of ACS is usually a vulnerable atherosclerotic plaque glycerin also may improve hypertension and symptoms of heart fail-
with either plaque rupture or plaque ulceration leading to thrombosis. ure, if present. Intravenous nitroglycerin therapy has not been proven
Unstable angina and NSTEMI are differentiated by pathologic elevation to improve mortality and usually is discontinued within 24 to 48 hours
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in the levels of cardiac biomarkers that confirm MI. of presentation. Patients who have taken drugs (e.g., sildenafil) for
Angina pectoris can be associated with other symptoms, such as erectile dysfunction within the preceding 24 hours are at increased risk
diaphoresis, dizziness, nausea, clamminess, and fatigue. Some patients for vasodilation and hypotension, so caution is advised in these patients
with ACS present with atypical symptoms rather than chest pain. The when intravenous nitroglycerin is given.
presentation may be dyspnea alone, nausea and/or vomiting, palpita- Reperfusion Therapy The overriding goal of treatment of
tions/syncope, or cardiac arrest. Rarely, patients with diabetes mellitus STEMI is restoration of myocardial blood flow and salvage of myo-
and other patients have a “silent MI” diagnosed incidentally on ECG or cardial tissue. A decision should be made immediately whether the
cardiac imaging study. patient will undergo a primary (direct) percutaneous coronary inter-
The initial ECG is often not diagnostic in patients with ACS. In vention (PCI) or receive a fibrinolytic agent. The currently preferred
one clinical study, the ECG was not diagnostic in approximately 45 per- approach is PCI, but the relative advantages and limitations of each
cent and was normal in 20 percent of patients who subsequently were therapy should be considered. The most important factor to consider
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shown to have experienced an acute MI. ST-segment elevation and is whether PCI is immediately available. Several randomized trials
Q waves are consistent with ST-segment elevation myocardial infarc- indicate enhanced survival with PCI compared to fibrinolysis, with a
tion (STEMI), but other conditions, such as acute pericarditis with early lower rate of intracranial hemorrhage and recurrent MI. 224,225 Transfer
repolarization variant and hypertrophic cardiomyopathy with Q waves, to a center that can provide PCI, if necessary, should be accomplished
may mimic the ECG manifestations of STEMI. in less than 2 hours. 226
Fibrinolytic therapy should be given immediately if PCI cannot
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Laboratory Features of Acute Myocardial Infarction be performed promptly. Prior to fibrinolysis, the patient should be
A variety of serum biomarkers are used to evaluate patients with sus- initially assessed for possible contraindications, which include active
pected acute MI. The three most commonly used tests are (1) troponin I bleeding, history of cerebrovascular disease, intracranial neoplasm,
and troponin T, (2) creatine kinase (CK) and its isoform CK-myocardial drug allergy, and trauma. A systolic blood pressure greater than 175 torr
band (MB), and (3) myoglobin. An elevated serum concentration of one is a relative contraindication but should not prohibit therapy, especially
or more of the three biomarkers is seen in almost all patients with acute if the pressure can be rapidly controlled. Many different fibrinolytic reg-
MI. The preferred biomarkers are the troponins because the troponin imens with different dosing schemes are available. Streptokinase was
assays are more specific than the other tests. the first thrombolytic agent tested but has proved less effective than
alteplase. In addition, streptokinase is antigenic and can cause an
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allergic reaction, particularly with repeat administration. Other throm-
Therapy for Acute Coronary Syndromes bolytic agents, such as tenecteplase and reteplase, have reportedly sim-
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Therapy for Acute Myocardial Infarction The initial management of ilar results compared to alteplase. Tenecteplase is popular on hospital
patients with STEMI depends upon prompt recognition and therapy to formularies because of its relatively easy single-bolus administration
reduce morbidity and mortality. A carefully coordinated plan of care is and reported lower rate of noncerebral bleeding. 229
essential for optimal results in patients with STEMI, given that multi- Anticoagulation Heparin, both unfractionated and low molecu-
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ple therapies usually are initiated simultaneously. The goals of therapy lar weight, is commonly used in patients with STEMI. The exact role
are to reduce ischemic pain, stabilize hemodynamic status, and quickly of heparin therapy with different fibrinolytic agents is evolving. Patients
establish myocardial reperfusion. The American College of Cardiology who undergo primary PCI usually are given unfractionated heparin
(ACC)/American Heart Association (AHA) guidelines for management 7500 U subcutaneously twice daily or low-molecular-weight heparin, for
of patients with acute MI are available at the ACC website. 222 example, enoxaparin, 1 mg/kg twice daily unless contraindications are
Antiplatelet Agents Unless contraindicated, all patients with evident. For patients receiving intravenous unfractionated heparin, the
acute MI should be given antiplatelet therapy. The Antiplatelet Trialists’ recommended dose is an initial 60 to 70 U/kg bolus (maximum: 5000 U)
Collaboration indicated a 30 percent reduction in vascular events with followed by 12 to 15 U/kg per hour (maximum: 1000 U/h) as continuous

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