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9. Currv SC, Vance MV, R\an PJ, et al: Envenomation In the scorpion Centruroides - ulpiuraiu» I Toxicology 1983-84; 21
10. Freire-Maia L, Campos )A, Amaral CF: Approaches to the treatment of scorpion envenoming. T >viccrs 1994, 32
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68
MANAGEMENT OF ACUTE CORONARY SYNDROME
ik iuvim/ of ibh mmIuaI liinfAii Kf i\ F\c,li4i liAkllifVl(>Ay^V R S.
CaiIimIua ol Emh«,kv\ Mulitix», PosiqKAdwm Docioiis Isuiiui*, AlMAiy RAkhiivil)Ayhv J.S.
Doc ion o( Fmh«.^\ly MkIkaI SiAiio\, suhsiAikw NNo 6, AImai\
Approximately 8 million patients present annually to the emergency room with symptoms ot acute chest pain. Of these,. 2 million turn out to have a cardiac cause resulting in hospitalization. Fewer than 10% of these patients have ST segment elevation on the electrocardiogram. Since the diagnostic sensitivity and spec ¡tic ity of the electrocardiogram are poor in this setting, there is a strong impetus tor effective emergency room stratification.
The spectrum of "Acute coronary syndromes" includes unstable angina and non-ST segment elevation myocardial infarction as the clinical presentations. The distinction between these syndromes is usually made retrospectively based on biochemical markers, and hence, initial treatment strategies are identical. The diagnosis of primary unstable angina excludes external factors that may exacerbate the symptoms of coronary ischemia, such as severe anemia, thyrotoxicosis, and tachyarrhythmias.
An approach to management must take into account the severity of symptoms, the circumstances in which they are occurring, and indicatory»!' the risk ot such catastrophic events as death or myocardial infarction.
Cli
inical Presentations of Unstable Angina
1. Rest angina
2. New onset angina of CCSC ( lass III or IV within 4 vvk of presentation
i. Increasing frequency and intensity of previously stable angina to CCSC class
III or IV
4. Angina within 6 wk of myocardial infarction (CCSC, Canadian Cardiovascular Society Classification). Braunwald Classification of Unstable Angina
Severity
Class I New-onset, severe, or accelerated angina
Patients with angina of less than 2 month duration, severe or occurring three or more times per day, or angina that is distinctly more frequent and precipitated by distinctly less exertion; no rest pain in the last 2 month.
Class II Angina at rest; subacute.
Patients with one or more episodes of angina at rest during 3 preceding months but not within the preceding 48 hours.
Class III Angina at rest; acute.
Patients with one or more episodes at rest within the preceding 48 hours.
Clinical Circumstances
Class A Secondary unstable angina.
A clearly identified condition extrinsic to the coronary vascular bed that has intensified myocardial ischemia, e.g., anemia, infection, fever, hypotension, tachyarrhythmia, thyrotoxicosis, hypoxemia secondary to respiratory failure.
Class B Primary unstable angina.
Class C Postinfarction unstable angina (within 1 week of documented myoc ardial infarction).
intensity of Treatment
1. Absence of treatment or minimal treatment.
116- // BecmHuk ATHyB. 2008, №1-2 (6-7)
2 1*1 urriog in present f oi standard therapy tfii i hi i>ni< iat>Ji- angina <tun\c-ntional (fuses di t»ibeta-blockers, nilraies and calcium antagonists!.
3. Occurring despite maximally tolerated doses ot all three c ategories of oral therapy, including nitroglycerin.
The term "'unstable angina" is currently falling into disuse and is being replaced with the term "Acute coronary syndrome without ST segment elevation" or, more simply, "Acute coronary syndrome."
This new nosology has developed for three reasons. First, the syndromes that do and do not cause ST segment elevation both have a common pathology, namely vascular inflammatory changes leading to disruption ofa previously stable atherosclerotic plaque, and subsequent thrombosis. The second reason for the adoption of the new terminology reflects the development of increasingly "sensitive" markers of myocardial necrosis. Patients with small amounts of myonecrosis as well as those with recent, rather than acute, episodes of necrosis who were previously classified as having "unstable angina" are n- recognized as having myocardial infarction Using the modern classification scheme ^>pou>cd b\ the joint European Sue etv it Card ologs/American College of CanJiu ' ¿aidelines. Third, effective forms or ih»„-'jpy cio n* it differ between patients a rh or without biochemical indications • r necrosis, bur rather are distinguished according to risk score and to the presence or absence of 5T segment elevation on the surface electrocardiogram.
The majority of patients presenting with non-ST segment elevation acute coronary s. dromes have multiple plaques in " e coionarv arteries. However, in most Mjdies. approximately 20% of patients u th suspected ac ute coronary syndromes v - round to have minimally obstructed or normal coronary arteries when coronary ir graphy is performed. This proportion :> s' »mt-what lower in studies that use more stringent entry criteria. The precipitating event of myocardial ischemia is most commonly coronary plaque disruption or erosion. Plaques vulnerable to this process tend to be relatively soft and lipid-rich, and have abundant extracellular matrix and smooth muscle t ells.
Following disruption of the fibrous cap. platelets are activated by local thrombogenic and inflammatory factors suc h as lipid and inflammatory mediators from Iipid4aden
macrophages. -\s a result thrombosis may ex i nr. The nnal component of arterial damage involves local vasoconstriction, most likely in response to secretion of platelet-derived serotonin and thromboxane A2.
Thrombolytic therapy has been shown to be ineffective, and potentially detrimental in non-ST segment elevation ac ute coronary syndromes. Treatment is based primarily on antithrombotic and antiplatelet agents.
The initial diagnosis of acute coronary syndrome (ACS) is based entirely on history, risk factors, and. to a lesser extent, ECG findings. The symptoms are due to myocardial ischemia, the underlying cause of which is an imbalance between supply and demand of myocardial oxygen.
Patients with ACS include those whose clinical presentations cover the following range of diagnoses: unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-ejevation myocardial infarction (STEMI). This ACS spectrum concept is a useful framework for developing therapeutic strategies.
Pathophysiology of ACS
Myocardial ischemia is most often due to atherosc lerotic plaques, which reduce the blood supply to a portion of myocardium. Initially, the plaques allow sufficient blood flow to match myocardial demand. When myocardial demand increases, the areas of narrowing may become clinically significant and precipitate angina. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest, and without recent change in frequency or severity of activity that produce symptoms, is called chronic stable angina. Overtime, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombus forms.
The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina. Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. Angiographic evidence of coronary thrombus formation may be seen in more than 90% of patients with STEMI but in only Iof patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI However, not every STEMI evolves into a Q-wave Ml; likewise, a patient with NSTEMI may develop Q waves.
The excessive mortality rate of coronary heart disease is primarily due to rupture
//Becmnuk AfHyB, 2008. №1-2(6-7) >117 «
and lhroinlx>ms cii the atheroM lerc>lit plaque. Inflammation plays a critical role in plaque destabilizalion and is widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome. Evidence indicates that platelets contribute to promoting plaque inflammation as well as thrombosis. A new theory of unbalanced cytokine-mediated inflammation is emerging, providing an opportunity for intervention.
A less common cause of angina is dynamic obstruc tion, which may be caused by intense focal spasm of a segment of an epicardial artery (Prinzmetal angina). Coronary vasospasm is a frequent complication in patients with connective tissue disease. Other causes include arterial inflammation and secondary unstable angina. Arterial inflammation may be caused by or related to infection. Secondary unstable angina occurs when the precipitating cause is extrinsic to the coronary arterial bed, sue h as fever, tachycardia, thyrotoxicosis, hypotension, anemia, or hypoxemia. Most patients who experience secondary unstable angina have chronic stable angina as a baseline medical condition.
Spontaneous and cocaine-related coronary artery dissection remains an unusual cause of ACS and should be included in the differential diagnosis, especially when a younger female or cocaine user is being evaluated. A;' early clinical suspic ion of this disease i* necessary for a good outcome. Cardiology consultation should be obtained for consideration for urgent percutaneous coronary intervention.
Irrespective ot the cause of unstable angina, the result of persistent ischemia is myocardial infarction (Ml).
History of the ACS:
Typically, angina is a symptom of myocardial ischemia that appears in circumstances of increased oxygen demand. It usually is described as a sensation of chest pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand.
Not all patients experience chest pain. Some present with only neck, jaw, ear, arm, or epigastric discomfort. Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalents.
A patient may present to the FD because of a c hange in pattern or severity of symptoms.
A new i as*- ut • - • < r K -k jfc
diagnose be< au>e rriu-t"-*^ .-'t -iie^ vague and similar Iu ir*j*e cawed fear^pM conditions e.g.. <.'- zr
Patients mav have nu u - ¿n ~u> complain of episodi-: -- i-sess fen weakness, lightheadei rv— ' =c s nausea and vomiting.
Patients may complain of ihe *■ tMammfd palpitations; pain, which i-^ . — i as pressure, squeezing or : burrrsr;|» sensation across the precord um ami may radiate to neck, shoulder, jaw hack upper abdomen, or either arm: exert ma dyspnea that resolves with pain or rt-: diaphoresis from sympathetic discharge nausea from vagal stimulation; decreased exercise tolerance; patients with diabetes and elderly patients are more likely to have atypical presentations and offer only vague complaints, suc h as weakness, dyspnea, lightheadedness, and nausea.
Stable angina: involves episodic pain lasting 5-15 minutes; provoked by exertion; relieved by rest or nitroglycerin.
Unstable angina. Patients have increased risk for adverse cardiac events, such as Ml or death. Three clinically distinct forms exist, as follows: new-onset exertional angina; angina of increasing frequency or duration or refractory to nitroglycerin; angina at rest; variant angina (Prinzmetal angina); occurs primarily at rest; triggered by smoking; thought to be due to coronary vasospasm.
Elderly persons and those with diabetes may have partic ularly subtle presentations and may complain of fatigue, syncope, or weakness. Elderly persons may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.
As many as half of cases of ACS are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Maintain a high index of suspicion for ACS especially when evaluating women, diabetics, older patients, patients with dementia, and those with a history of heart failure.
Physical findings:
Physical examination results are frequently normal. If chest pain is ongoing, the patient usually will lie quietly in bed and may appear anxious, diaphoretic, and pale. Hypertension may precipitate angina 01 relief I elevated c alec holammes due to either
•118 • // BecmHuk AfHyB, 2008. N° 1-2 (6-7)
anxiety 01 exogenous sympathnrMimeti slinutlat.on Hypotension indicates wmiituldf tiysiufKtklo due to rtyocanfial ischemia, in'arctum. or acute valvular dysiundm It K possible Jo find <wt signs ofc ngpsfi'.t' tart fat lure iCHF and mgular venous fibteottnfiL Sometmtes one. an I tear third heart sound <S3.i. A new. murmur mav reiler papillary muscJt- dysfunction. Raies on pulmonary examination arc sujjgestrng left ventricular (LV) dysfunction or mitral regurgitation. Presence of a fourth heart sound iS4) is a common finding in patients with poor ventricular compliance due to preexisting ischemic heart disease or hypertension.
Causes of the ACS:
1. Atherosclerotic plaque is the predominant cause. Coronary artery vasospasm is less common.
2. Alternative causes of angina include the following: ventricular hypertrophy due to hypertension, valvular disease, or cardiomyopathy: embolic: occlusion of the coronary arteries; hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders; cocaine and amphetamines, which increase myocardial oxygen demand and may cause coronary vasospasm; underlying coronary artery disease, which ma>» be unmasked by severe anemia: inflammation of epicardial arteries; coronary arterv dissection.
Risk factors for ACS should be documented and include the following: male gender; diabetes mellitus (DM); smoking history; hypertension; increased age: hypercholesterolemia; Hyperlipemia; prior cerebrovascular accident (CVA) - these patients constitute 7.5% of patients with ACS and have high-risk features; inherited metabolic disorders; methamphetamine use; occupational stress; connective tissue disease.
Laboratory studies and findings:
Troponin I is considered the preferred biomatker for diagnosing myocardial necrosis. Troponins have the greatest sensitivity and specificity in detecting Ml, and elevated serum levels are considered diagnostic of Ml. They also have prognostic value. For early detection of myocardial necrosis, sensitivity of troponin is su|>erior to that of the creatine kinase-MB (CK-MB). Troponin I is detectable in serum 3-6 hours after an Ml, and its level remains elevated for 14 clays. Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial nec rosis
Ifoponiti <hould be used as the •jplimnm iv "Tvrkeis lor the evaluation
(*aii'Tit> with \CS who have coexistent skeletal muscle <n|urv.
Troponin T has similar release kinetics ro uoovun I and remains elevated foi i4 days. False-positive results may occur in oaiien's v.'itl • rena failure. Minor elevations ¡n UQixrnin T aiso identify patients at risk for subsequent cardiac events. Elevated troponin levels may also point to minoi myocardial injury due to other causes.
CK-MB levels hegin to rise within 4 hours after Ml, peak at 18-24 hours, and subside over 3-4 days. A level within the reference range does not exclude myocardial necrosis. The upper limit of normal for CK-MB is 5-6% of total CK. A normal level in the ED (Emergency Department) does not exclude the possibility of Ml. A single assay in the ED has a 34% sensitivity for Ml. Serial sampling over periods of 6-9 hours increases sensitivity lo approximately 90%. Serial CK-MB over 24 hours detects myocardial necrosis with sensitivity near 100% and a specificity of 98%. Occasionally, a very small infarct will be missed by CK-MB; therefore, troponin levels should be measured foi patients suspected to have Ml who have negative results from serial CK-MB tests.
Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as 2 hours after Ml. Myoglobin levels, although highly sensitive, are not cardiac specific. They may be useful for early detection of Ml when performed with other studies.
Cardiac markers should be used liberally to evaluate patients with prolonged episodes of ischemic, pain, with new changes on ECG, or with nondiagnostic or normal ECGs in whom the diagnosis of ACS or Ml is being considered.
Complete blood count is indicated to determine if anemia is a precipitant. Transfusion with packed red blood cells may be indicated.
Chemistry profile: Obtain a basic metabolic profile, including a check of blood sugar level, renal function, and electrolytes levels, foi patients with new-onset angina. Potassium and magnesium levels should be monitored and corrected. Creatinine levels must be considered before using an angiotensin-converting enzyme (ACE) inhibitor. Imaging Studies:
//Вестник АГИУВ. 2008. № 1-2 (6-7) -119 «
Chest radiograph may demonstrate complications of ischemia. such a\ pulmonary edema, or provide clues 10 alternative causes or symptoms such 3-thoracic aneurysm or pneumonia.
Echocardiogram often demons^ates wall motion abnormalities due to ischemia. It is of limited value in patients whose symptoms have resolved or in those with preexisting wall motion abnormalities. However, echocardiogram mav lie useful in identifying precipitants for ischemia, such as ventricular hypertrophy and valvular disease.
ECG is the most important ED diagnostic test tor angina. It may show changes during symptoms and in response to treatment, which would confirm a cardiac basis for symptoms. It also may demonstrate preexisting structural or ischemic heart disease (left ventricular hypertrophy, Q waves). A normal ECG or one that remains unchanged from the baseline does not exclude the possibility that chest pain is ischemic in origin. Treatment of the ACS
Prehospital Care: Generally, patients transported with chest pain should initially be managed under the assumption that the pain is ischemic in origin. Prehospital interventions should be guided by the nature of the presenting complaint, individual risk factors, and associated symptoms (e.g., breathing difficulty, hemodynamic instability, appearance of ectqpyj. Airway, breathing, and circulation should be rapidly assessecL'.vith institution of CPR, ACLS-guided interventions, or other measures as indicated for the unstable patient.
Management:
I. Obtain IV access.
1. Administer supplemental oxygen.
3. Aspirin should be given in the field, 162-325 mg chewed and swallowed.
4. Prehospital ECG, if available, may be helpful in selected circumstances.
5. Perform pulse oximetry.
6. Administer sublingual or aerosolized nitroglycerin if chest pain is ongoing and is felt to be cardiac in origin.
Emergency Department Care:
Antithrombin therapy and antiplatelet therapy should be administered to all patients with an ACS regardless of the presence' or the absence of ST-segment elevation. Patients presenting with persistent ST-segment elevation are candidates foi reperfusion therapy (either pharmacological or catheter
Ixjsc-ii ' jreport- iUm [>n>m|.rtl\ in(tieuciliMlet! epicariJial infarct-1 eialed arieiy. Patients presenting v. • *om ST—element elevation are
nc" cancl»ciare> t vallate pharmacological
reperfusion bul 1 receive anti-ischemic iherapv when appr^^^e. Management:
T. GoalsorED; t --r identification of patients tl >Ttv exclusion ot alternative causes of r - - hemic chest pain, andstratnerr: n . ha ute
coronary ischemia into kwv- and high-risk groups.
2. Obtain iV ac e-- " -ter supplemental oxygen anc> pm . v. \ monitoring if these procedures -rave not already been accomp! shea in prehospital phase. In addition, obtain a 12-lead ECG as soon as possible are- . .
3. Complete a history and physical examination, with focus on risk factors for coronary ischemia; onset, duration and pattern of symptoms; and early ideniir.c anon of complications of myocardial ischemia (e.g., new murmurs, cardiac congestive-failure).
4. Perform frequent reassessment of vital signs and symptoms in response to administered therapies.
5. Serial ECGs and continuous ST segment monitoring may be useful.
6. Medical therapy.
The goals of treatment are to preserve patency of the coronary artery, augment blood flow through stenotic lesions, and reduce myocardial oxygen demand. All patients should receive antiplatelet agents, and patients with evidence of ongoing ischemia should receive aggressive medical intervention until signs of ischemia, as determined by symptoms and LCG, resolve.
Drug Category:
Antiplatelet agents - Inhibit the cyclooxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator. Antiplatelet therapy has been shown to reduce mortality by reducing the risk of fatal strokes and fatal myocardial infarctions.
Nitrates - These agents oppose coronary artery spasm and reduce myocardial oxygen demand by reducing both preload and afterload.
Analgesics These agents reduce pain which decreases sympathetic stress, in addition to providing some preload reduction.
Antic oaj>ulan's - These agents are
-120 < // BecmHuk AmyB. 2008. № 1-2 (6-7)
lActl lo pev.t<v Raí une» •
■ .vi.
Heia-atUeneigpc fcfcrkeí-These agents have ant a¡rrh.*r in £<>Tih)pertensive projX'rties aw.r ¿ -¿- . to reduce ischemia T! wrerrt/«-■ imbalance between " . - - * - m «V» inn demand by redw: " - c stress. In patients nrrth acato Ml if*> have been <howr t n e-: — • • <¡2t well as srrr- ar. rr ii , v\htch
is a tuner ir v tvir ar' - ^-"emic and aniiatrhv"^^ irm.* —
Low tr - u eight lepar in
(en<;.vap3* has >—- s^oa i to reduce cardiac s£%mi c evtrrs and dean by as muc/1 as 5 . ~ pj6en:> w>ih unstable angina. Une cfiakai efccts have been repose r -x i : - ¿'so receiving aspirin.
Di^eci - - -- rs - h-'udin is the p< i ft fifi wf-^Mtdwambtn inhibitors. Hirudin hearts srpc" » v Sr arr . .->n binding site anr --«■ c: ■s.ie? a* thrombin
to or . : _ -r d predictable
antic^atüár zr
- -nr: - vi ADP receptor arr _ - " c-nrvv ii *»es, ticlopidine
c V - - ^ ^agonists that - "t cr re^- activity. Both
ha. z rr«evers-c e ¿-- ; iatel^t activity but ' * í - ---- \ v ,> «o Tie manifest. A f • nerefit ex. sts when ADP
M^túb an? used m conjunction with aspirin. These (ftrugs mav l>e considered atosvahm to aspirin in patients intolerant
' io? alter or allergic lo aspirin.
High-risk criteria include the following:
1. Symptoms refractory to medical management
2. Hemodynamic instability,cardiogenic shock
3. New or worsening mitral regurgitant murmur
4. Known oi suspected severe aortic stenosis
Complications:
1. Acute myocardial infarction
2. Cardiogenic shock
3. Ischemic mitral regurgitation
4. Arrhythmias: a) supraventricular arrhythmias (rare complication of ischemia, may actually pre< ipitate ischemic events); b) ventricular arrhythmias; simple and complex premature ventricular contractions (PVCs), and nonsustained ventricular tachycardia.
5. Atrioventricular nodal blockade: usually transient in setting of reversible ischemia; treatment guided by location of block and hemodynamic stability.
6. Ventricular rupture occurs in the interventricular septum or the LV free wall. This represents a catastrophic event with mortality rates greater than 90%. Prompt recognition, stabilization, and surgical repair are crucial to any hope of survival. An echocardiogram usually will define the abnormality, and a right heart catheterization may show an oxygenation increase with septal rupture.
References:
§агтн В a. Sheps DS, Monroe S, et al: A population-based evaluation of the thrombolysis in
m -.г: ± rrarct n ->k score for unstable angina and non-ST elevation myocardial infarction. Clinical Cardk*»«v 2004 Feb.
. Sraurmald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed., 2007
. -: «ascular Emergencies. Edited by Crispin Davies and Yaver Bashir. BMJ, 2001
- : 35cwi3- Medicine. Edited by Willerson et al. Springer, 2007
* С * -ar\ Heart Disease in Clinical Practice. Satish Mittal. Springer, 2005
ь. Сал-ihi v M, Lanipe FC, Wood DA: Incidence, clinical characteristics, and short-term prognosis of angina pectons »rrtain Heart journal, 1995 Feb.
7. Heif D -ease Diagnosis and Therapy. Khan. Humana Pres, 2005.
~ amm С Ra\ kilde J. Cerhardt W, et al: The prognostic value of serum troponin T in unstable angina. Чем Eagtand Journal Medicine, 1992 Jul 16.
Нз-di D, Haim M. Behar S, et al: Acute coronary syndromes in patients with prior cerebrovascular events: lessor?» - тп the Euro-Heart Survey of Acute Coronary Syndromes. American Heart journal, 2003 Nov.
■ s the Heart. Ed. Valentin Fuster et al. McGraw-Hill, 2004
* 1 Ijnriah В Venge P. Wallentin L: Relation between troponin T and the risk of subsequent cardiac events л umtjh - coronary arterv disease. The FRISC study group. Circulation 1996 May 1.
; v nasemc-nt of Acute Coronary Syndromes. Ed. Cannon. Humana Press. 2003
R „5 Gomez |A. Fiol M, et al: Spontaneous coronary artery dissection causing acute coronary syndrome: an ear . с a<^no>is implies a good prognosis. American Journal Emergency Medicine, 2003 Nov.
: - 7 a. or s Cardiovascular Diseases. Taylor et al. Springer, 2005
1 - Te*rhnok of Cardiovascular Medicine. Ed. Topol et al. Williams-Wilkins, 2007
p. W и AH Abbas SA, Green S: Prognostic value of cardiac troponin T in unstable angina pectoris. American Journal Cardiology, 1995 Nov 1.
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