ENFERMEDAD CORONARIA

Sndrome Coronario agudo: es un espectro de presentaciones clnicas que se

clasifican como angina inestable, IAM sin elevacin del S-T e IAM con elevacin
del S-T. Ocurren bsicamente por ateroesclerosis y disminucin de la oxigenacin
en el territorio de las ramas coronarias.

Las demandas de oxgeno dependen de la FC, PAS (postcarga), estrs de la

pared (vol diastlico finalxmasa miocrdica), contractibilidad

Doble producto: FC x PAS representa la demanda de oxgeno, se produce angina

en el ejercicio cuando se supera el doble producto absoluto.

Hay aumento de la demanda de oxgeno en cualquier condicin con aumento de

catecolaminas o tono simptico, estrs, taquicardia, HT, hipertrofia del ventrculo
izquierdo (con cardiopata hipertensiva o estenosis aortica)

Hay disminucin de la oferta cuando hay ateroesclerosis, vasoespasmos,

enfermedad de la microvasculatura coronaria, hipertrofia del ventrculo izquierdo
que puede terminar en disminucin del fluo subendocardico y la oferta de oxgeno
terminando en angina.

1) Angina pectoris: isquemia miocrdica asociada a disnea, nauseas, diaforesis,

fatiga.
Se conoce como la angina clsica aquella que presenta dolor torcico opresivo, no
punzante (pensar en dolor pleurtico), que puede irradiarse a epigastrio, hombro,
cuello, mandibula y regin interescapular, que puede ser desencadenado por la
actividad fsica, el estrs, coito, comida, decbito, cocana ocurre sobretodo en la
maana por aumento del tono simptico y mejora en reposo o con nitroglicerina.
La angina estable es aquella que no presenta cambios en el patrn en por lo
menos 60d.

La angina tpica se conoce como la angina que se presenta con cualquiera de

esas 3 caractersticas (dolor de duracin corta que es provocada por esfuerzos y
mejora en reposo), la angina atpica es aquella que presenta 2/3 de estas
caractersticas y si no presenta ninguna hay que pensar en dolor torcico no
cardaco.

Al examen fsico hay: aumento de la PA, taquicardia, taquipnea, diaforesis,

regurgitacin mitral o de estenosis aortica en caso de cardiopata hipertensiva,
signos de hiperlipidemia (arco corneal y xantelasmas), puede haber signos de IC
como R3, estertores, aumento de PVY y edema.

En el ECG puede haber depresin del S-T

Tratamiento:
-Aspirina 75-162mg/d o clopidogrel 75mg/d
-Betabloqueante sin ASI: incia con dosis baja y a las dos semanas se aumenta
hasta obtener FC entre 50-60lpm
-BCC tipo DHP: no nifedipina por taquicardia refleja
-Nitroglicerina sublingual
-IECA/ARAII

2)Angina inestable e IAM sin elevacin del S-T:

La angina inestable se caracteriza por angina en reposo de mas de 20min, nueva

aparicin de angina o modificacin del patrn de angina preexistente con mayor
duracin, no cede en reposo. No hay elevacin de enzimas cardacas y puede o
no haber cambios electrocardiogrficos como depresin del S-T, elevacin de
onda T transitoria o nueva inversin de onda T.

El IAM sin elevacin del S-T se presenta igual que la angina inestable pero con
aumento de enzimas cardacas (por encima del 99% de su valor referencial),
sobretodo en pacientes mayores de 65 aos tienen mas riesgo de presentar
NSTEMI que STEMI. Pacientes mayores tienden a tener presentaciones atpicas
como infartos silentes, sincope, confusin, debilidad.

Se debe realizar un ECG a los 10min del ingreso y medir enzimas cardacas, las
tropininas sricas en especial la troponina I son ms especificas que el resto de
las enzimas cardacas al msculo cardaco. Existe una highly sensitive troponina I
hsTnI o troponina I contempornea que puede ser determinada a las 3h del inicio
de los sntomas en comparacin de las 6h.

Tratamiento:
1. Oxigeno en pacientes con saturacin menor de 90%
2. Nitroglicerina sublingual y comenzar EV posterior a 3 dosis sublinguales
3. Morfina como manejo del dolor intolerable, ya que se ha visto que aumenta
la mortalidad en estos pacientes NSTEMI por interacciones con
antiagregantes.
-2-8mg en intervalos entre 5-15min
Betabloqueantes EV dentro de las primeras 24horas en pacientes sin IC ni
signos de bajo gasto.
Metoprolol :5 mg rapid IV q2min, up to 3 doses; then, 15 minutes after last
IV, 50 mg PO q6hr for 48 hours; then 50-100 mg PO q12hr
If full IV dose not tolerated: 25-50 mg PO q6hr after last IV

Atenolol: dosis EV??

A cardioselective oral beta blocker, such as metoprolol or atenolol, is
preferred in the setting of an acute myocardial infarction (MI). We use oral
metoprolol tartrate 25 to 50 mg every 6 to 12 hours or atenolol 25 to 50 mg
twice daily, initially, titrating upward as needed. Short-acting beta blockers
are preferred early to allow for more rapid adjustment of dose based on the
patients blood pressure and heart rate response. Near the time of
discharge, we prefer to switch to longer-acting beta blockers.
 For the uncommon patient in whom intravenous therapy may be chosen,
such as those with ongoing ischemia prior to PCI in whom there is no
hemodynamic instability including heart failure, we suggest the following
regimens [17] (see 'Primary PCI' above):
Intravenous metoprolol tartrate can be given in 5 mg increments by slow
intravenous administration (5 mg over one to two minutes), repeated every
five minutes for a total initial dose of 15 mg (three doses). Patients who
tolerate this regimen should then receive maintenance oral therapy with
metoprolol succinate 50 mg daily beginning 15 min after the last intravenous
dose.

Intravenous atenolol can be given in a 5 mg dose followed by another 5 mg

five minutes later. Patients who tolerate this regimen should then receive
maintenance oral therapy with atenolol 50 mg twice daily beginning one to
two hours after the last intravenous dose. Intravenous atenolol is not
available in the United States or Canada.

Esmolol (50 mcg/kg per min increasing to a maximum of 200 to 300 mcg/kg
per min), an ultra-short-acting beta blocker, can be given to assess
tolerance to beta blockade in patients with borderline or questionable left
ventricular function.

Bradycardia and hypotension are the most common limitations to achieving

the full dose. In this setting, the rate of administration should be slowed or
oral therapy initiated. However, a rigid "cookbook" regimen should not be
used since there is a variable sympathetic response to acute MI.

4. BCC no DHP en caso de contraindicacin de betabloqueantes

5. Initial antiplatelet/anticoagulant therapy includes 325-mg chewable aspirin at
presentation, followed by a daily maintenance dose of aspirin at 81-126 mg
daily. A P2Y12 inhibitor (clopidogrel or ticagrelor) should be used in addition
to aspirin for up to 12 mo in patients treated with either an early-invasive or
ischemia-guided strategy. In addition to antiplatelet therapy, parenteral
anticoagulation is indicated with enoxaparin, bivalirudin, fondaparinux, or
unfractionated heparin.
Aspirin blocks cyclooxygenase (prostaglandin H synthase), the enzyme that
mediates the first step in the biosynthesis of prostaglandins and
thromboxanes (including TxA2) from arachidonic acid (figure 3), que es un
potente estimulador proagregante.

The P2Y12 receptor blockers, clopidogrel, ticlopidine, prasugrel, ticagrelor,

and cangrelor block the binding of adenosine diphosphate (ADP) to a
platelet receptor P2Y12, thereby inhibiting activation of the glycoprotein
(GP) IIb/IIIa complex and platelet aggregation [1].
 Anti-GP IIb/IIIa antibodies and receptor antagonists inhibit the final common
pathway of platelet aggregation (the cross-bridging of platelets by fibrinogen
binding to the GP IIb/IIIa receptor) and may also prevent adhesion to the
vessel wall.

Se recomienda terapia dual con aspirina e inhibidor de P2Y12 por lo menos

por un ao en aquellos pacientes con sx coronario agudo. (CURE TRIAL).
El estudio PCI-CURE secundo el beneficio de terapia dual previo a PCI
-Terapia con aspirina se inicia dosis de 162-300mg y la primera tableta se
debe masticar o crushed para mayor absorcin, seguido de mantenimiento
75-100mg OD de forma indefinida como prevencin secundaria.
-Terapia con bloqueantes del receptor plaquetario P2Y12 (clopidogrel,
ticlopidine, prasugrel, ticagrelor, cangrelor) Ticlopidine is rarely chosen due
to the risk of thrombocytopenia, neutropenia, and gastrointestinal
intolerance. Three limitations to the use of clopidogrel (delayed onset of
action, large between individual variability in platelet response, and
irreversibility of its inhibitory effect on platelets) led to the development of
other agents, including prasugrel and ticagrelor [7]. Both prasugrel and
ticagrelor induce more intense platelet inhibition than clopidogrel and have
been found to be both more effective and associated with higher rates of
bleeding. In all trials of P2Y12 receptor blockers, these drugs have been
given in conjunction with aspirin.
In addition, evidence from TRITON-TIMI 38 (prasugrel) and PLATO
(ticagrelor) provides strong support for the general idea that agents with
higher levels of platelet inhibition have lower cardiovascular event rates but
higher rates of bleeding compared to clopidogrel [23].
6. Dosis: bolo de 300mg de clopidogrel seguido de 75mg/dia de 3-12meses,
sin embargo la terapia dual con clopidogrel aumento el riesgo de
sangramiento
7. Anticoagulacin: se recomienda anticoagulacin en todo paciente posterior
a un evento coronario en estudios que compararon anticoagulantes vs
placebo.

HEPARINS inhibidores indirectos de trombina al unirse con la

antitrombina (III) generando cambios conformacionales modificando su
accin de inactivadora lenta a rapida, inactivan factor Xa. Se ha
comprobado que heparinas de bajo peso molecular como enoxaparina
tienen major resultado en comparacin con heparinas no fraccionadas.
In these trials, the usual dose of enoxaparin was 1 mg/kg every 12 hours
and for UFH was 60 U/kg initial bolus, followed by an infusion of 12 U/kg per
hour (adjusted to a goal activated partial thromboplastin time [aPTT] of 1.5
to 2.0 times the upper limit of normal or 50 to 70 seconds). Treatment was
generally started soon after the diagnosis and continued for two and eight
days, unless otherwise noted.
The ESSENCE trial compared the effectiveness enoxaparin to continuous
intravenous UFH in 3171 aspirin treated patients with unstable angina
(angina at rest) or acute NSTEMI; therapy was given for a minimum of 48
hours to a maximum of eight days [7]. Revascularization was not intended in
this trial. At 30 days, enoxaparin therapy had a significant lower rate of a
combined end point of death, MI, and recurrent angina (19.8 versus 23.3
percent with UFH) or a revascularization procedure (27.0 versus 32.2
percent). There was no difference between the two groups in the rates of
major bleeding (6.5 versus 7.0 percent) or severe thrombocytopenia (0.4
versus 0.6 percent) [8]. These benefits were maintained at one year for both
the combined end point (32 versus 36 percent) and the need for repeat
revascularization (36 versus 41 percent) [9]. Approximately one-third of
patients underwent percutaneous coronary revascularization or coronary
artery bypass graft surgery.
The benefits of enoxaparin compared to UFH in UA or NSTEMI were
confirmed in the TIMI 11B trial of 3910 aspirin treated patients for whom
revascularization was not intended [10]. The incidence of the primary end
point (death, MI, or urgent revascularization) was significantly lower with
enoxaparin at eight days (12.4 versus 14.5 for heparin). The benefit of
enoxaparin was limited to patients with elevated levels of troponin I [11].

The incidence of major bleeding was greater with enoxaparin (0.9 versus 0.4
percent with UFH; p = 05), but there was no increase in transfusion rates.

Most patients with non-ST ACS are treated with dual antiplatelet therapy
(aspirin plus a platelet P2Y12 receptor antagonist or GP IIb/IIIa inhibitor) in
addition to anticoagulant. Thus, the three trials presented above are not
directly applicable to current care. The SYNERGY trial provides the best
evidence with which to compare UFH to enoxaparin in patients who receive
contemporary antiplatelet therapy [13,14]. This trial randomly assigned
10,027 patients with a non-ST elevation ACS for whom an early invasive
management strategy was planned to open label enoxaparin or UFH.
Concomitant medications in SYNERGY included aspirin (95 percent),
clopidogrel or ticlopidine (66 percent), and a GP IIb/IIIa inhibitor (57 percent).
Coronary angiography was performed in 92 percent of the SYNERGY
patients; 47 percent underwent PCI and 19 percent underwent surgical
revascularization. In many patients, anticoagulant therapy was stopped after
PCI.The following findings were noted:

-There was no significant difference in the rate of the primary end point of
death or nonfatal MI at 30 days or at six months with enoxaparin (14.0
versus 14.5 percent and 17.6 versus 17.8 percent, enoxaparin compared to
UFH). There was also no difference in death or nonfatal MI or in all-cause
mortality at one year (7.4 versus 7.8 percent).
-There was a significant increase in in-hospital major bleeding with
enoxaparin (9.1 versus 7.6 percent for UFH). Both cardiovascular and
bleeding outcomes were worse in patients initially treated with either
enoxaparin or UFH and then switched to the other agent compared to
patients who did not switch.
The results from SYNERGY suggest that, in patients with a non-ST elevation ACS
who receive an oral platelet P2Y12 receptor blocker and aspirin (and a GP IIb/IIIa
inhibitor in some cases) and undergo PCI, enoxaparin and UFH have comparable
efficacy. However, enoxaparin is associated with a significant increase in major
bleeding.
Other LMWHs Other LMWHs, including nadroparin, tinzaparin, and dalteparin
have been compared to placebo, UFH, or enoxaparin. These drugs appear to have
equivalent efficacy to UFH, may be less effective than enoxaparin, and may be
associated with higher rates of major bleeding.
Heparins summary Enoxaparin and UFH appear to be of equal efficacy when
patients with UA and NSTEMI are evaluated in the aggregate. However, patients
who are managed by a conservative strategy (ESSENCE, TIMI 11B, and Phase A
of the A to Z trials) appear to have fewer adverse cardiovascular events when
treated with enoxaparin compared to UFH. In addition, enoxaparin is easier to
administer (subcutaneous as opposed the intravenous route with UFH) and
requires no laboratory monitoring. (PORQUE NO PROLONGA TIEMPOS)
On the other hand, for patients undergoing an early invasive strategy, UFH may be
preferable in patients at high bleeding risk due to the increased risk of bleeding
(table 1) with enoxaparin seen in the SYNERGY trial. There is no evidence to
support the use of other LMWHs in preference to enoxaparin.
DIRECT THROMBIN INHIBITORS The efficacy and safety of the direct
thrombin (IIa) inhibitors (argatroban, inogatran, efegatran, hirudin, and bivalirudin
[Hirulog]), have been evaluated in trials of patients with non-ST elevation acute
coronary syndrome (ACS). A meta-analysis of early trials found a significantly lower
risk of death or MI at 30 days with direct thrombin inhibitors compared to heparin
(7.4 versus 8.2 percent with unfractionated heparin [UFH], odds ratio 0.91, 95% CI
0.84-0.99), which was primarily due to a reduction in MI [22]. The treatment benefit
was seen with hirudin and bivalirudin, but not with inogatran or argatroban. The
better outcome was significant only in patients who underwent early PCI [23].
Compared to UFH, the risk of major bleeding (table 1) was increased with hirudin
and reduced with bivalirudin; there was no difference in intracranial hemorrhage.
FACTOR XA INHIBITORS
Fondaparinux Fondaparinux is a reasonable anticoagulant choice in ACS
patients, particularly those at increased risk of bleeding (table 1), based principally
on the results of the OASIS-5 trial.
In OASIS-5, 20,078 NSTEACS patients were randomly assigned to fondaparinux
(2.5 mg/day) or enoxaparin (1 mg/kg twice daily) for a mean of six days
(anticoagulant was generally stopped after PCI, if it was performed) [32-35]. Over
60 percent of patients underwent catheterization and over 30 percent had
percutaneous coronary intervention (PCI). Patients received weight-adjusted UFH
during PCI if the last dose of enoxaparin was greater than six hours before the
procedure. For patients who received an initial dose of subcutaneous fondaparinux
and then underwent PCI, an additional dose was given intravenously (table 3).
After isolated reports of catheter thrombosis, a protocol amendment allowed for the
addition of open-label UFH in patients receiving fondaparinux at the discretion of
the investigator.
The two groups had similar rates of the primary end point, defined as death,
myocardial infarction (MI), or refractory ischemia at nine days (5.8 versus 5.7
percent with enoxaparin), and the secondary end point of death or MI (4.1 percent
in both groups).
At longer term follow-up, there was a reduction in the primary end point with
fondaparinux at 30 days (2.9 versus 3.5 percent, hazard ratio 0.83, 95% CI 0.71-
0.97) and six months (5.8 versus 6.5 percent, hazard ratio 0.89, 95% CI 0.81-1.00).
These differences were entirely due to a significantly lower rate of death.

The safety of fondaparinux relative to enoxaparin was confirmed in two important

prespecified subgroups:
In the 6238 patients who underwent PCI, fondaparinux significantly reduced major
bleeding at day nine (2.4 versus 5.1 percent, hazard ratio 0.46, 95% CI 0.35-0.61),
with comparable rates of the combined end point of death, MI or stroke [34].

Fondaparinux significantly reduced major bleeding in the 3630 patients who

received glycoprotein IIb/IIIa inhibitors and the 13,531 patients who received
platelet P2Y12 receptor blockers (5.2 versus 8.2 percent, hazard ratio 0.46, 95%
CI 0.35-0.61 and 3.4 versus 5.4 percent, hazard ratio 0.62, 95% CI 0.52-0.73
respectively) [35]. Ischemic events were similar between the two treatment arms in
these two subsets, as in the entire OASIS-5 population. In addition, these findings
regarding safety and efficacy were similar in the 3246 patients who received both
antiplatelet therapies.

However, fondaparinux was associated with a small but significant increase in

catheter-related thrombi (in patients undergoing PCI) compared to enoxaparin (0.9
versus 0.4 percent). The frequency of catheter related thrombi was significantly
reduced in both groups in those patients who received open-label UFH before the
procedure.
The observation in the OASIS-5 trial of a small but significant increase in catheter-
related thrombi, which was mitigated by the use of UFH, raises the question as to
the optimal dose of UFH in such patients. This issue was directly addressed in the
FUTURA/OASIS 8 trial in which 2026 high-risk patients with non-ST elevation
acute coronary syndromes treated with fondaparinux and scheduled to undergo
PCI within 72 hours were randomly assigned to either a standard dose UFH
regimen (85 units/kg bolus with additional boluses based on an activated clotting
time dosing algorithm) or a fixed low dose (50 units/kg without activated clotting
time) [36]. For patients receiving a glycoprotein IIb/IIIa inhibitor, the UFH bolus in
the standard-dose group was lowered to 50 units/kg.
At 48 hours after PCI, there was no significant difference between low-dose and
standard regimens in the rate of the primary composite endpoint of major bleeding,
minor bleeding, or major vascular access-site complications (4.7 versus 5.8
percent, respectively). The composite secondary outcome of major bleeding at 48
hours with death, myocardial infarction, or target vessel revascularization within 30
days occurred more often in the low-dose group, nearly attaining statistical
significance (5.8 versus 3.9 percent; odds ratio 1.51, 95% CI 1.00-2.28). Catheter
thrombus rates were very low and not statistically different in the two groups (0.5
and 0.1 percent, respectively). (See "Periprocedural bleeding in patients
undergoing percutaneous coronary intervention".)
Otamixaban The TAO trial randomly assigned 13,229 patients with NSTEACS
scheduled to undergo an early invasive strategy to the investigational drug
otamixaban or unfractionated heparin plus eptifibatide [37]. There was no
significant difference between the two strategies in the rate of the primary
composite efficacy outcome of all-cause death or new MI through day seven, but
the rate of the bleeding was greater with otamixaban.
Factor Xa summary Fondaparinux is a reasonable anticoagulant option to
UFH, enoxaparin, or bivalirudin for patients with non-ST elevation ACS:
For patients managed with a conservative strategy, we prefer fondaparinux or
enoxaparin to unfractionated heparin or bivalirudin. Issues of cost and local
practice may influence the choice between the two. We prefer fondaparinux to
enoxaparin in patients at increased risk of bleeding (table 1), based on the findings
in OASIS-5.

For those patients undergoing PCI in whom fondaparinux was chosen as the initial
anticoagulant, we recommend switching to standard dose UFH, with further dosing
of the latter based on the activated clotting time, as was done in the
FUTURA/OASIS 8 trial. Although bivalirudin has not been evaluated in this setting,
we believe that switching to bivalirudin is also a reasonable anticoagulant strategy.

We do not recommend using otamixaban for these patients.

ANTICOAGULANT REGIMENS
Dose The initial dosing schedules are as follows
UFH Intravenous bolus of 60-70 units/kg (maximum dose 5000 units)
 followed by 12 units/kg per hour intravenously to achieve an activated partial
thromboplastin time of 50 to 75 seconds.

-Enoxaparin No loading dose is necessary. Dosing is 1 mg/kg

subcutaneously every 12 hours or for patients with an estimated creatinine
clearance less than 30 mL/min, 1 mg/kg subcutaneously daily.

-Fondaparinux 2.5 mg subcutaneously once daily in patients managed with

a non-invasive strategy. (See 'Fondaparinux' above.)

-Bivalirudin Intravenous bolus of 0.1 mg/kg and an infusion of 0.25 mg/kg

per hour before angiography; if PCI is performed, an additional 0.5 mg/kg
bolus is given and the infusion rate is increased to 1.75 mg/kg per hour.

-If fondaparinux was initiated, UFH in standard dose (50 U/kg bolus, with an
ACT goal of greater than 200 seconds) or bivalirudin in standard dose is
given. (See 'Fondaparinux' above.)

Duration The duration of anticoagulant therapy depends on the initial

management strategy. Although the optimal treatment length has not been
determined, the following represent commonly employed regimens in clinical
practice (which we consider reasonable):
-For patients undergoing PCI, anticoagulant therapy is stopped at the end of the
procedure in uncomplicated cases. Continuation of anticoagulation beyond the
times suggested above should be undertaken only if:

The PCI is complicated and there is an ongoing risk or recurrent ischemia.

SUMMARY AND RECOMMENDATIONS Anticoagulant therapy with either

bivalirudin, fondaparinux, unfractionated heparin (UFH), or enoxaparin prevents
thrombus related ischemic events in patients with non-ST elevation acute coronary
syndromes (ACS), which includes unstable angina and non-ST elevation
myocardial infarction (NSTEMI). The following are our recommendations for the
use of anticoagulants in patients with non-ST elevation ACS:
1. We recommend anticoagulant therapy for all patients (Grade 1A). (See
'Anticoagulant versus placebo' above.) This recommendation is made for
patients irrespective of whether an invasive or a conservative approach is
taken. Anticoagulant therapy should be given as soon as possible after
diagnosis and should be given in conjunction with recommended antiplatelet
therapy. (See 'Approach to anticoagulation' above and "Antiplatelet agents
in acute non-ST elevation acute coronary syndromes", section on 'Summary
 and recommendations'.)

2. For patients managed with an early invasive strategy (angiography within 4

to 48 hours), we suggest bivalirudin or UFH as opposed to enoxaparin
(Grade 2B) or to fondaparinux (Grade 2C). When fondaparinux is chosen,
UFH (or bivalirudin) should be given before percutaneous coronary
intervention.

3. For patients who will be referred to the catheterization laboratory within four
hours (usually due to patient instability for reasons such as refractory
angina, heart failure, arrhythmia, or hemodynamic instability), we
recommend UFH or bivalirudin as opposed to fondaparinux or enoxaparin
(Grade 1B). (See 'Approach to anticoagulation' above.) We suggest UFH in
preference to bivalirudin (Grade 2B). This recommendation assumes that
patients will receive a potent oral antiplatelet agent (ticagrelor or prasugrel),
which we prefer to clopidogrel. For those patients who receive clopidogrel,
either UFH or bivalirudin is a reasonable choice. In addition, patients at high
bleeding risk are reasonable candidates for bivalirudin.

4. For patients in whom a conservative (noninvasive) strategy is planned, we

recommend either fondaparinux or enoxaparin in preference to either
unfractionated heparin or bivalirudin (Grade 1B). (See 'Heparins summary'
above and 'Factor Xa summary' above and 'Direct thrombin inhibitors
summary' above and 'Approach to anticoagulation' above.)The choice
between fondaparinux and enoxaparin should be guided by issues of cost
and local practice. For patients at higher risk of bleeding (table 1), we
suggest fondaparinux (Grade 2B). (See 'Enoxaparin versus UFH' above
and 'Factor Xa summary' above.)

5. The dosing schedules and duration of therapy for these anticoagulants are
discussed above. (See 'Anticoagulant regimens' above.)

8. Estatinas:
Atorvastatina 80mg/dia

TIMI risk score Analysis of data from the TIMI 11B and ESSENCE trials found
that seven variables at presentation were independently predictive of outcome in
patients with unstable angina or an acute non-ST elevation myocardial infarction
(MI); a value of one was assigned when a factor was present and 0 when it was
absent (calculator 1) [40]:
1. Age 65 years
 2. Presence of at least three risk factors for coronary heart disease
(hypertension, diabetes, dyslipidemia, smoking, or positive family history of
early MI).
3. Prior coronary stenosis of 50 percent
4. Presence of ST segment deviation on admission electrocardiogram
5. At least two anginal episodes in prior 24 hours
6. Elevated serum cardiac biomarkers
7. Use of aspirin in prior seven days (which is probably a marker for more
severe coronary disease) [41]

Patients are considered to be at low risk with a score of 0 to 2, intermediate risk

with a score of 3 to 4, and high risk with a score of 5 to 7 (figure 1).

Infarto agudo del miocardio con elevacin del S-T

Deteccin de elevacin o cada de los valores de biomarcadores cardacos
(preferiblemente troponina cardaca [cTn] con un valor por encima del lmite
superior del percentil 99, ms cualquiera de los siguientes:
Sntomas de isquemia
Ondas Q patolgicas en el ECG
Cambios nuevos o presuntamente nuevos del segmento ST onda T o
signos recientes de bloqueo de rama izquierda
Identificacin de un trombo intracoronario mediante angiografa o autopsia
Evidencia imageneolgica de prdida reciente de miocardio o
anormalidades recientes del movimiento de la pared cardaca
Muerte cardaca con sntomas sugestivos de isquemia cardaca y nuevos cambios
isqumicos en el ECG o un nuevo bloqueo de rama izquierda; pero la muerte
ocurri antes de obtener los resultados de los biomarcadores o antes de que
incrementaran.

Escala de Killip
I ausencia de signos de ICC mortalidad de 6%
II R3 y/o estertores pulmonares mortalidad 17%
III edema agudo de pulmn 30-40%
IV shock cardiogenico 60-80%

Escala de timi

Diagnostico:
-Hematologia, PT, PTT, INR,
-qumica y electrolitos
-tipiaje
-Enzimas cardacas: mioglobina es la primera en elevarse (1-2h pico 6-8 horas y
dura hasta 24h, poca especificidad), CK confirma lesin miocrdica en primeras
48h y la mortalidad es directamente proporcional (se eleva de 2-6h pico de 12-18 y
dura hasta 48h), troponias I y T son ms especificas se elevan de 3-6h, pico 24-36
hasta 14d.

-ECG:

Criterios del ECG para Dx:

Nueva elevacin del segmento ST en el punto J en dos derivaciones contiguas
con punto de corte: >0.1 mV (1mm) en todas las derivaciones menos en V2-V3.
Para V2-V3, aplican los diguientes puntos de corte: 0.2 mV (2mm) en hombres
40 aos, 0.25 mV en hombres <40 aos, o 0.15 mV en mujeres
generalmente las ondas Q se observan en pacientes ms jvenes y en pacientes
mayores o con corazones ms enfermos no se produce onda Q por lo que es de
peor pronostico.

-Isquemia: riego sanguneo menor que el normal, se observa onda T invertida y

simtrica (e observa en angina inestable y NSTEMI) si no es simtrica se habla de
engrosamiento de cavidades
-Lesin aguda: elevacin del segmento S-T representando infarto agudo (mayor
de 4mm)
la depresin del segmento S-T puede ocurrir en infartos subendocardicos o en
 intoxicacin por digitalicos.
-Necrosis: Onda Q patolgica: mas de 0.04s o 1/3 de la altura del QRS, mala
progresin de la R

en caso de ondas Q o elevacin del ST es infarto anterior, depresin del ST y

ondas R grandes (sobretodo en V1 que las R suelen ser pequeas) infarto
posterior.

En caso de bloqueo de rama izquierda, el corazn izquierdo se despolariza

despus que el derecho, por lo tanto ya no es posible ver al principio del complejo
QRS una onda Q producida por el ventrculo izquierdo por lo cual existen los
criterios de sgarbossa:

] ST elevation 1 mm in a lead with a positive QRS complex (ie: concordance) - 5

points
] ST depression 1 mm in lead V1, V2, or V3 - 3 points
] ST elevation 5 mm in a lead with a negative (discordant) QRS complex - 2 points
3 points = 90% specificity of STEMI (sensitivity of 36%)[2]
Smith modified Sgarbossa rule:
] at least one lead with concordant STE (Sgarbossa criterion 1) or
] at least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2)
or
] proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S
ratio of equal to or more than 0.20 and at least 2 mm of STE. (this replaces
Sgarbossa criterion 3 which uses an absolute of 5mm)
Wackers et al. correlated ECG changes in LBBB with localization of the infarct by
thallium scintigraphy.[7] The most useful ECG criteria were:
Serial ECG changes 67 percent sensitivity
ST segment elevation 54 percent sensitivity
Abnormal Q waves 31 percent sensitivity
Cabrera's sign 27 percent sensitivity, 47 percent for anteroseptal MI
Initial positivity in V1 with a Q wave in V6 20 percent sensitivity but 100 percent
specificity for anteroseptal MI

-px con depresin del ST en V1-V3 y elevacin del ST en pred inferior u onda R
altas evaluar pared posterior
-Depresin reciproca del ST opuesta al territorio del infarto aumenta especificidad
en IAM

V1-V6 pared anterior y septal A. Descendente anterior izquierda proximal

V1-V2 tabique A. Descendente anterior izquierda proximal
V2-V4 pared anterior A. Descendente anterior izquierda
V5-V6 pared lateral A. Circunfleja izquierda
II, III, aVF pared inferior ACI o ACD
I, aVL pared lateral anterior

TRATAMIENTO AGUDO

1. Oxgeno en pacientes que estn saturando menos de 90%, distress

respiratorio, insuficiencia cardaca y alto riesgo de hipoxia
2. Nitratos: usar nitroglicerina EV si el dolor precordial persiste despus de 3
nitroglicerina sublingual en caso que no haya riesgo de hipotensin severa
3. Morfina: se reserva en pacientes con dolor intorelable ya que se ha
demostrado un aumento en la tasa de mortalidad
se diluye una ampolla en 9cc de solucin y se pasan 3cc inicialmente y
posteriormente 2cc cada 20minutos, tiene interaccin con antiagregantes
plaquetarios
4. Terapia antiplaquetaria:
-aspirina: dosis en bolo de 300mg (VER NSTEMI) resulto en disminucin de
la mortalidad. En pacientes tomando tricagrelor la dosis de aspirina debe
ser menor de 100mg. La aspirina se continua INDEFINIDAMENTE EN
PREVENCION SECUNDARIA
EA: efectos gastrointestinales, sangrado, asma y broncoespasmo (alergia),
u otro sangrado externo al tracto GI. Pacientes que presenten trastornos
gastrointestinales tratarlos con inhibidores de bomba de protones y asi
toleraran bajas dosis.
-se recomienda que a todos los pacientes que vayan a recibir tratamiento
fibrinolitico reciban terapia antiplaquetaria dual (aspirina e inhibidor P2Y)
con clopidogrel (dosis de 600) no hay evidencia que respalde terapia dual
con inhibidores GP IIb/IIIa y el uso de fibrinoliticos. El ticagrelor y prasugel
tienen mayor terapia antiplaquetaria y se recomiendan mas si el paciente va
a PCI.
RESUMEN
There is strong evidence to support the early initiation of dual antiplatelet
therapy with aspirin and a platelet P2Y12 receptor blocker, irrespective of
treatment strategy (fibrinolysis, primary percutaneous coronary intervention
[PCI], or medical therapy), in patients with acute ST-elevation myocardial
infarction (STEMI). There is a limited role for intravenous glycoprotein (GP)
IIb/IIIa inhibitor therapy in patients with planned primary PCI, and no role in
patients receiving fibrinolytic therapy or those not undergoing reperfusion.
Our recommendations for the early use of antiplatelet therapy in patients
with STEMI follow; recommendations for the long-term use of these drugs
are found elsewhere.
All patients

-We recommend aspirin (and a platelet P2Y12 receptor blocker) as soon as

possible after presentation (Grade 1A). (See 'Aspirin for all patients' above.)
The first aspirin tablet should contain 162 to 325 mg and be chewed. The
recommended maintenance dose of aspirin is 75 to 81 mg/day; when
ticagrelor is used, the dose must be less than 100 mg/day. (See 'Aspirin for
all patients' above.)
-For those patients with a history of gastrointestinal bleeding, drugs that
reduce the risk of recurrent bleeding (eg, proton pump inhibitors) should be
given. (See "Periprocedural and long-term gastrointestinal bleeding in
patients undergoing percutaneous coronary intervention", section on
'Summary and recommendations'.)
Fibrinolytic therapy

-For patients receiving fibrinolytic therapy, we recommend clopidogrel in

preference to ticagrelor or prasugrel (Grade 1C). Neither the efficacy nor the
safety of ticagrelor or prasugrel in conjunction with fibrinolytic therapy has
been evaluated and there is a potential for life-threatening bleeding (eg,
intracranial hemorrhage). (See 'With fibrinolytic therapy' above.)The
suggested loading dose of clopidogrel is 300 mg for those who are less than
75 years of age. For patients 75 years of age or older, clopidogrel 75 mg
loading dose should be given (table 1).
-We recommend not using a GP IIb/IIIa inhibitor in these patients. (See 'With
fibrinolytic therapy' above.)

Primary PCI

-For patients with planned primary PCI, we suggest ticagrelor or prasugrel in

preference to clopidogrel (Grade 2B). The loading dose for ticagrelor is 180
mg and for prasugrel is 60 mg (table 1). Prasugrel is contraindicated in
patients with prior stroke or transient ischemic attack, and both prasugrel or
ticagrelor are contraindicated in those with active pathological bleeding.
(See 'With primary PCI' above.) For those patients in whom clopidogrel is
chosen, we recommend a loading dose of 600 mg as opposed to 300 mg
(Grade 1B). We then start 75 mg daily. For patients treated with either
drug-eluting or bare metal stents who are not at high bleeding risk and who
do not have planned noncardiac surgery within one year, we recommend
dual antiplatelet therapy (DAPT) for at least 12 months rather than a shorter
treatment duration (Grade 1B). Practitioners should evaluate patients after
the first 12 months of DAPT to be certain that there has not been major
bleeding or other important difficulty related to DAPT. For patients who have
had a complication of DAPT, continuation after 12 months may not be
appropriate. For patients who have not had a significant complication with
DAPT during the first 12 months, we suggest continuing such therapy for an
additional 36 months (Grade 2B). (See 'Duration' above.)
For most patients undergoing primary PCI and who receive early antiplatelet
therapy with aspirin and a P2Y12 inhibitor, we recommend not routinely
using a GP IIb/IIIa inhibitor (Grade 1B). (See 'Glycoprotein IIb/IIIa inhibitors'
above.)
-For patients treated with heparin who do not receive a P2Y12 receptor
blocker prior to PCI, we recommend the addition of a GP IIb/IIIa inhibitor, as
opposed to not adding this agent, after diagnostic angiography (Grade 1B).
 UpToDates authors and reviewers have differing preferences (for
abciximab, tirofiban, or eptifibatide) in this setting. (See 'Glycoprotein IIb/IIIa
inhibitors' above.)
-For patients who receive bivalirudin, we suggest not routinely adding GP
IIb/IIIa inhibitor therapy (Grade 2B). (See "Anticoagulant therapy in acute
ST elevation myocardial infarction", section on 'UFH compared to
bivalirudin'.)
No reperfusion therapy
-For patients receiving neither fibrinolytic therapy nor primary PCI, we
suggest ticagrelor in preference to clopidogrel or prasugrel (Grade 2C).
(See 'No reperfusion' above.)
5. Anticoagulacin:
Heparina no fraccionada dosis bolo 60U/kg maximo 4000U mantener
anticoagulado por 8d

Enoxaparina: dosis inicial en bolo de 30mg seguido de 1mg/kg SC BID (no

mas de 8d) en pacientes mayors de 75 aos no se da bolo sino que se da
0.75mg/kg BID

All patients with ST-elevation myocardial infarction should be treated with

anticoagulant therapy, which should be given as soon as possible after
diagnosis. The choice of anticoagulant agent depends upon the treatment
strategy for each patient. The dosing and duration for these drugs
(unfractionated heparin [UFH], low molecular weight heparin, bivalirudin, or
fondaparinux) are presented above. (See 'Anticoagulant regimens' above.)

For patients treated with primary percutaneous coronary intervention

(PCI), we recommend anticoagulant therapy (Grade 1B). (See 'Primary PCI'
above.)

-We suggest UFH in preference to bivalirudin (Grade 2B). This

recommendation assumes that patients will receive a potent oral antiplatelet
agent (ticagrelor or prasugrel), which we prefer to clopidogrel. For those
patients who receive clopidogrel, either heparin or bivalirudin is a
reasonable choice. In addition, patients at high bleeding risk are reasonable
candidates for bivalirudin. (See 'Primary PCI' above.)

-For patients treated with fibrinolytic therapy, we suggest anticoagulant

therapy (Grade 2B). (See 'Fibrinolytic therapy' above.)

-For patients not at high risk of bleeding, we suggest using enoxaparin as

opposed to UFH, fondaparinux, or bivalirudin (Grade 2C). For those patients
in whom PCI is possible or likely after fibrinolytic therapy, UFH is a
reasonable choice.
For patients at high risk of a bleeding complication and who are not likely to
require PCI, we suggest fondaparinux as opposed to enoxaparin or UFH
(Grade 2C). (See 'Fondaparinux' above and 'Fibrinolytic therapy' above
For patients treated without reperfusion, we suggest anticoagulant therapy
with enoxaparin or UFH as opposed to no anticoagulant therapy, as soon as
possible after presentation (Grade 2B). We do not use fondaparinux or
bivalirudin in this setting. (See 'No reperfusion therapy' above.)
ANTICOAGULANT REGIMENS
Dose The dosing schedules depend upon the clinical situation [45-50]:
Unfractionated heparin (UFH):
For patients receiving fibrinolysis, we suggest an intravenous bolus of 60 to
100 units/kg (maximum of 4000 units) followed by 12 units/kg/hour
(maximum 1000 units/hour) intravenously to achieve an activated partial
thromboplastin time of 50 to 70 seconds.

For patients undergoing primary percutaneous coronary intervention (PCI)

and who are treated with heparin, we suggest an intravenous bolus of 50 to
70 units/kg up to a maximum of 5000 units (target activated clotting time
[ACT] >250 seconds). For patients who receive a glycoprotein inhibitor, we
aim for an ACT of >200 seconds.

For patients treated with medical therapy (no reperfusion), we suggest an

intravenous [IV] bolus of 50 to 70 units/kg up to a maximum of 5000 units, to
be followed by an IV drip of 12 units/kg per hour, with a goal aPTT of 1.5 to
2 times control or approximately 50 to 75 seconds.

Enoxaparin:
For patients treated with fibrinolysis or no reperfusion therapy, and who are
<75 years of age, we use a loading dose of 30 mg IV bolus followed by 1
mg/kg subcutaneously every 12 hours (maximum of 100 mg for the first two
doses only). The first subcutaneous dose should be administered with the IV
bolus. In patients 75 years, we use no loading dose and 0.75 mg/kg
subcutaneously every 12 hours (maximum of 75 mg for the first two doses
only). Adjustment for renal impairment: For patients with a creatinine
clearance <30 mL/minute using the Cockroft-Gault formula and who are <75
years of age, we use a 30 mg IV bolus given with the first dose of the
subcutaneous maintenance regimen, which is adjusted to 1 mg/kg
subcutaneously every 24 hours. For patients who are 75 years or older with
a creatinine clearance <30 mL/minute, we omit the intravenous bolus and
give a maintenance subcutaneous dose of 1 mg/kg every 24 hours.

Repeated doses of low molecular weight heparin to patients with renal

impairment may lead to accumulation and increased risk of bleeding to
varying degrees. In contrast, unfractionated heparin is not dependent
primarily upon renal function for clearance and is a preferred option for
patients with creatinine clearance <20 mL/min, kidney failure, or receiving
dialysis

For patients who will receive PCI after multiple doses of therapeutic
subcutaneous enoxaparin, we give a supplemental IV bolus dose of 0.3
mg/kg of enoxaparin if the last subcutaneous dose was 8 to 12 hours earlier
or if only one subcutaneous dose has been administered; no additional IV
bolus dose is given if the last subcutaneous dose was within the preceding
eight hours [51,52]. For patients who will receive PCI more than 12 hours
after the last dose of therapeutic subcutaneous enoxaparin, we prefer UFH
[52].

For patients undergoing primary PCI, we generally prefer UFH. For patients
undergoing primary PCI with a radial artery approach, an intravenous bolus
of 0.5 mg/kg of enoxaparin (with an additional bolus of 0.25 mg/kg if the
procedure is prolonged by more than two hours) can be used.

Fondaparinux:

For patients being managed medically, we suggest giving 2.5 mg

intravenously, followed by 2.5 mg subcutaneously once daily. Fondaparinux
is not approved by the United States Food and Drug Administration for this
use. Fondaparinux should be avoided in patients with estimated creatinine
clearance less than 30 mL/minute.

Fondaparinux is not recommended for use in patients undergoing primary

PCI. For patients undergoing PCI who were treated with fondaparinux,
intravenous heparin or bivalirudin should be given during the procedure to
prevent catheter-related thrombosis. (See 'Classification of anticoagulant
agents' above.)

For patients receiving fibrinolytic therapy, we give 2.5 mg intravenously as a

bolus followed by a subcutaneous dose of 2.5 mg once daily.
Bivalirudin We suggest an initial bolus of 0.75 mg/kg followed by an
intravenous infusion of 1.75 mg/kg per hour. Administration of UFH or low
molecular weight heparin (LMWH) prior to arrival in the catheterization
laboratory for primary PCI is not a contraindication to transitioning to
bivalirudin during the procedure.

Duration The duration of anticoagulant therapy depends on the initial

management strategy. Although the optimal treatment length has not been
determined for these, the following represent commonly employed regimens
in clinical practice:
For patients undergoing PCI, heparin is stopped at the end of the procedure
in uncomplicated cases. Some of our experts stop bivalirudin at the end of
the procedure while others continue bivalirudin at a dose of 1.75 mg/kg/hour
for four hours after the procedure based on findings from the EUROMAX
trial reported in abstract form [53,54]. In that abstract, the rate of acute stent
thrombosis was lower with this higher dose than with a dose of 0.25
mg/kg/hour. (See 'UFH compared to bivalirudin' above.)
For patients receiving fibrinolytic therapy or no reperfusion therapy, UFH is
continued for at least two days; if LMWH or fondaparinux are used, therapy
 should be continued preferably for up to eight days or until hospital
discharge, whichever occurs earlier.
Continuation of anticoagulation beyond the times suggested above should
be undertaken only if:
The PCI is complicated and there is an ongoing risk of recurrent ischemia
There is evidence of high risk for systemic or venous thromboembolism (eg,
anterior STEMI, severe left ventricular dysfunction, heart failure, history of
systemic or pulmonary embolus, or echocardiographic evidence of left
ventricular thrombus) or a pre-existent rational for long-term anticoagulation,
such as patients with prosthetic heart valves or atrial fibrillation.
6. Terapia fibrinolitica:

Si es menos de dos horas desde inicio de sintomatologia se realiza PCI o

terapia fibrinolitica a dosis maxima
mas de dos horas PCI

The 2013 American College of Cardiology Foundation/American Heart

Association guideline for the management of STEMI recommends the use of
fibrinolytic therapy in patients with symptom onset within 12 hours who
cannot receive primary percutaneous coronary intervention within 120
minutes of first medical contact (table 2A-B) [4,5]. The time interval from
hospital arrival to initiation of fibrinolytic drug infusion should be less than 30
minutes

Fibrinolytic therapy has generally not improved outcomes in patients

presenting at 12 hours or later and is therefore not indicated in those who
are stable and asymptomatic. However, fibrinolysis can be considered up to
24 hours after symptom onset if the patient has ongoing or stuttering chest
pain and PCI is not available

Primary percutaneous coronary intervention (PCI) is the preferred

reperfusion strategy for most patients with acute ST elevation myocardial
infarction (STEMI). When timely primary PCI is not available, early
fibrinolysis should be carried out. (See 'Fibrinolysis versus primary PCI'
above.)

We make the following recommendations for the use of fibrinolytic therapy in

patients with acute STEMI:

For patients within 12 hours of the onset of STEMI who have no absolute
contraindications to fibrinolytic therapy and for whom reperfusion with
primary PCI cannot be performed within the recommended time, we
recommend fibrinolytic therapy as opposed to no reperfusion therapy
(Grade 1A). (See 'Indications for fibrinolytic therapy' above.)

For symptomatic patients who present after 12 (but before 24) hours of
symptom onset and when PCI is not readily available, we suggest fibrinolytic
therapy as opposed to no reperfusion therapy (Grade 2B).

We recommend prehospital as opposed to in-hospital administration of

fibrinolytic therapy for patients with acute STEMI in whom a decision has
been made to not use primary PCI as the reperfusion strategy (Grade 1A)
This recommendation applies only to patients in health-care settings where
prehospital administration of fibrinolytic therapy is feasible. (See 'Timing'
above.)

Irrespective of whether fibrinolytic therapy is given prehospital or in the

hospital (emergency department), it should be started within 30 minutes
after the diagnosis of STEMI is made. (See 'Timing' above.)

We recommend a fibrin-specific agent instead of streptokinase (Grade 1B).

We suggest tenecteplase instead of alteplase or reteplase (Grade 2B).

Early transfer to a PCI center after fibrinolysis should be recommended to

decide whether rescue or elective PCI are necessary. (See 'Management
after fibrinolysis' above.)

Choice of agent We prefer fibrin-specific agents to streptokinase and we

prefer tenecteplase to other fibrin-specific agents based on its generally
favorable benefit-to-risk profile and its ease of use (table 1). The following
conclusions regarding available agents have been reached from
randomized trials and support our choice of tenecteplase (see
"Characteristics of fibrinolytic (thrombolytic) agents and clinical trials in acute
ST elevation myocardial infarction"):

Alteplase improves survival compared with streptokinase (streptokinase is

not available in the United States or Canada). 15mg en bolo, 0.75mg/kg
Reteplase is comparable to alteplase.
Tenecteplase has comparable efficacy to alteplase, but has a lower rate of
noncerebral bleeding events and is easier to use [33]. It is given as a single
bolus and is therefore easier to administer than alteplase, which requires a
bolus and then two separate drips.
Estreptocinasa: mas barato, mayor potencial fibrinolitico que ocurre
tardiamente, se diluyen 1.5millones de unidades en 100cc de solucin
dextrosada a razn de 30cc/hora
 CI: en pacientes con depresin del ST, con 5 o ms factores de riesgo de
hemorragia, pueden ocasionar arritmias por reperfusin que solo se tratan
si hay inestabilidad hemodinmica
7. Estatinas; atorvastatina 80mg/dia

TRATAMIENTO CRONICO

1. Betabloqueante cardioselectivo
2. Nitratos
3. Estatinas
4. Bloqueantes de canales de calcio
5. Espironolactona
6. Aspirina 81mg OD mas clopidogrel 75mg OD

PREGUNTARON EN CLASE TRATAMIENTO DE TAQUICARDIA VENTRICULAR,

COLGAJO DE TAQUICARDIA VENTRICULAR (LIDOCAINA ?)