1. Sindromi Coronariche Acute
Terapia

2. Terapia in STEMI
Riperfusione e Rivascolarizzazione
Terapia medica

3. Gestione pre-ospedaliera dello STEMI
5 min
≤90 min PCI
≤30 min fibrinolisi
Eur Heart J 2012;33:

4. Gestione pre-ospedaliera dello STEMI
Eur Heart J 2012;33:

5. Gestione dello STEMI Oppiodi per il dolore
Ossigeno in pz con ipossia ( SaO2 <95%), dispnea o scompenso cardiaco acuto
Tranquillanti in pz molto ansiosi
Arresto cardiaco
Defibrillatore
Training in Cardiac Life Support
Monitoraggio ECG al punto di primo contatto medico
Ipotermia terapetica subito dopo la resuscitazione, pz comatosi
Angiografia immediata
Eur Heart J 2012;33:

6. Reperfusion Therapy: STEMI
Fibrinolysis
Primary PCI

7. Rivascolarizzazione: Fibrinolisi
IIa
IIb
III A
Entro 12 h dalla sintomatologia, in assenza di controindicazioni e quando la PCI primaria non può essere effettuata entro 120 min dal FMC B
In pz. che si presentano entro 2 h dalla sintomatologia, con infarti larghi e rischio di emorragia basso, se il tempo dal FMC al ballon è >90 min A
Fibrinolisi pre-ospedaliera B
Agente fibro-specifico
Eur Heart J 2012;33:

8. Agenti fibrinolitici Non fibrino specifici Streptokinasi (SK)
Alteplase (t-PA)
Reteplase (r-PA)
Tenecteplase

9. Controindications to fibrinolytic therapy
Absolute controindications
Haemorrhagic stroke or stroke of unknown origin at any time
Ischaemic stroke preceding 6 months
Central nervous system trauma or neoplasma
Recent major trauma/surgery/head injury (within preceding 3 weeks)
Gastro-intestinal bleeding within the last month
Known bleeding disorder
Aortic dissection
Non-compressible punctusres (e.g. liver biopsy, lumbar puncture)
Eur Heart J 2012;33:

10. Controindications to fibrinolytic therapy
Relative controindications
Transiet ischaemic attack in preceding 6 months
Oral anticoagulant therapy
Rpregnancy or within 1 week post partum
Refractory hypertension (SBP > 180 mm HG and/or DBP > 110 mm HG)
Advanced liver disease
Infective endocarditis
Active peptic ulcer
Refractory resuscitation
Eur Heart J 2012;33:

11. Doses of Fibrinolytic Agents
Initial treatment
Specific contraindications
Streptokinase (SK)
1.5 milions units over min i.v.
Prior SK or anistreplase
Alteplase (t-PA)
15 mg i.v. bolus
0.75 mg/kg over 30 min then
0.5 mg/kg over 60 min i.v.
Total dosage not exceed 100 mg
Reteplase (r-PA)
10 U + 10 U i.v. bolus given 30 min apart
Tenecteplase
Single i.v. bolus
30 mg if < 60 kg
35 mg if <70 kg
40 mg if < 80 kg
45 mg if <90 kg
50 mg if ≥ 90 kg
Eur Heart J 2012;33:

12. Fibrinolytic therapy: Adjunctive Therapies
Antiplatelet antagonist:
if not already on Aspirin oral or soluble or chewable/ no enteric-coated) or i.v. dose of aspirin
Clopidogrel loading dose if age ≤ 75 years
if age > 75 years
Antithrombin co-therapy with alteplase, reteplase and tenecteplase
Enoxaparin i.v. bolus followed 15 min. later by first s.c. dose, if age > 75 years no i.v. bolus and start with reduced first s.c. dose.
UFH i.v.( a weight-adjusted bolus) followed by a weight adjusted i.v. infusion with first aPTT control after 3 h (if Enoxaparin is not available)
Eur Heart J 2012;33:

13. Interventi dopo la fibrinolisi
Angiografia in emergenza nei pz. con scompenso cardiaco/shock
Angiografia dopo fibrinolisi
Tempistica ottimale dell’angiografia in pz. stabili dopo fibrinolisi di successo è 3-24 h
Eur Heart J 2012;33:

14. Rivascolarizzazione: STEMI
Eur Heart J 2012;33:

15. Reperfusion Therapy: Primary PCI
IIa
IIb
III
Indicated in all patients with chest pain/discomfort of < 12 hrs and with persistent ST-segment elevation or (presumed) new LBBB A
Should be considered if there is clinical and/or ECG evidence of ongoing ischemia if symptoms started > 12 hrs before C
Reperfusion (PCI) in stable patients presenting > 12hrs to 24 hrs after symptom onset B
PCI totally occluded infarcted artery in stable patients > 24 hrs after symptom onset without signs of ischemia is not recommended A
Eur Heart J 2012;33:

16. Reperfusion Therapy: Primary PCI
IIa
IIb
III A
Preferred reperfusion treatment if performed by an experienced team as soon as possible within 120 min of FMC
Indicated for patients with cardiogenic shock and those with contraindications to fibrinolytic therapy irrespective of time delay B
RESCUE PCI
After failed fibronolysis in pts with large infarcts performed within 12 hrs A
Eur Heart J 2012;33:

17. Dye strongly persistent
TIMI Myocardial Perfusion (TMP) Grades
TMP Grade 3
TMP Grade 2
TMP Grade 1
TMP Grade 0
Normal ground glass
appearance of blush
Dye mildly persistent
at end of washout
Dye strongly persistent
at end of washout
Gone by next injection
Stain present
Blush persists
on next injection
No or minimal blush
6.2%
p = 0.05
5.1%
4.4%
Mortality (%)
2.0%
n = 434
n = 79
n = 46
n = 203
Gibson et al, Circulation 1999

18. Advantages of Primary PCI
Higher initial reperfusion rates
Lower recurrence rates of ischemia / infarction
Less residual stenosis
Less intracranial bleeding
Defines coronary anatomy and LV function
Utility when fibrinolysis contraindicated

19. Stents in STEMI A A Stenting is recommended (over balloon angioplasty
IIa
IIb
III A
Stenting is recommended (over balloon angioplasty
alone for primary PCI) I
IIa
IIb
III A
Drug-eluting Stent (DES) as an alternative to a
bare metal stent (BMS) for primary PCI in STEMI
* Consideration for the use of stents (DES or BMS) in STEMI should include the ability of the patient to comply with prolonged dual antiplatelet therapy, the bleeding risk in patients on chronic oral anticoagulation, and the possibility that the patient may need surgery during the ensuing year
Eur Heart J 2012;33: 19

20. PCI for unprotected left main
PCI of the LM coronary artery using stents as an
alternative to CABG may be considered in patients
with isolated LM or LM plus single vessel disease, for
pts. with ostial lesions and for pts. with co-morbidities
(such as severe lung disease, prior thoracic surgery or
poor CABG targets) that would make CABG high risk
or unlikely to be successful I
IIa
IIb
III B *
Conversely, CABG for uLMCA may be relatively more favorable for patients with LMCA plus multi-vessel disease, distal/bifurcation LMCA lesions, or low surgical risk with good chance of technical success. 20

21. Primary PCI: Adjunctive Therapies
Antiplatelet antagonist
Aspirin oral or i.v.
ADP receptor blocker in addition to aspirin
Clopidogrel
Prasugrel, in naïve clopidogrel pts., if no history of stroke/TIA, age<75 yrs.
Ticagrelor
GPIIb/IIIa antagonist
abciximab
tirofiban
eptifibatide
Antithrombin co-therapy
Enoxaparin
Unfractioned heparin
Bivalirudin
Fondaparinux
Adjunctive devices
Thrombus aspiration
Eur Heart J 2012;33:

22. ISIS-2 (Second International Study of Infarct Survival)
Collaborative Group
N=17187
Lancet 1988;2:349-60

23. TIMI Major NonCABG Bleeds
STEMI Cohort N=3534
TRITON TIMI-38 15
CV Death / MI / Stroke
Clopidogrel
12.4%
9.5%
10.0% 10
HR 0.79
Percent (%)
( )
6.5%
Prasugrel
P=0.02
NNT = 42
HR 0.68
( ) 5
P=0.002
TIMI Major NonCABG Bleeds
Prasugrel
2.4
2.1
Clopidogrel 30 60 90
180
270
360
450
Days From Randomization
Montalescot et al Lancet 2008.Adapted with permission from Antman EM. 23

24. Terapie di routine nella fase acuta, subacuta e a lungo termine: STEMI
Aspirina (mantenimento mg/die)
Eparine
Prasugrel/Ticagrelor/Clopidogrel ( se PCI, dose mantenimento)
Anticoagulanti orali ( se pz von valvole prostetiche, FA)
Beta-bloccanti ( NO in ipotensione)
Ca-antagonisti ( se beta-bloccanti controindicati)
Ace-inibitori/ ARBs
Statine ad alte dosi
Antagonisti dei recettori del aldosterone

25. Treatment Strategy for Right Ventricular Ischemia/Infarction
Maintain right ventricular preload
Volume loading (IV normal saline)
Avoid use of nitrates and diuretics
Maintain AV synchrony (AV sequential pacing for symptomatic high-degree heart block unresponsive to atropine)
Prompt cardioversion for hemodynamically significant SVT
Inotropic support
Dobutamine (if cardiac output fails to increase after volume loading)

26. Terapia in UA/NSTEMI
Early Conservative Strategy?
Vs.
Early Invasive Strategy?

27. Early Conservative Versus Invasive Strategies
Two different treatment strategies, termed “early conservative” and “early invasive” have evolved for patients with UA/NSTEMI.
In the early conservative strategy, coronary angiogrpahy is reserved for patients with evidence of recurrent ischemia (angina or ST-segment changes at rest or with minimal activity) or a strongly positive stress test despite vigorous medical therapy.
In the early invasive strategy, patients without clinically obvious contraindications to coronary revascularization are routinely recommended for early coronary angiography and angiographically directed revascularization if possible.

28. Early Invasive Strategy
Coronary angiography
class I - Level Evidence A
Early Invasive Strategy
Recurrent angina-ischemia at rest or with low level activities despite intensive anti-ischemic therapy
Elevated TnT or TnI
New or presumably new ST-segment depression
Recurrent angina/ischemia with CHF symptoms
High-risk findings on noninvasive stress testing
Depressed LV systolic function
Hemodynamic Instability
Sustained Ventricular Tachycardia
PCI within 6 months
Prior CABG
ACC/AHA Practice Guidelines

29. Early Conservative Strategy
Coronary angiography is reserved for patients with:
Evidence of recurrent ischemia
- angina at rest or with minimal activity
- dynamic ST-segment changes
Strongly positive stress-test
(despite vigorous medical therapy)
ACC/AHA Practice Guidelines

30. Comparison of Outcomes (death or MI in non-Q-wave MI):
VANQWISH
25%
24%
20%
18.6%
15%
10.4%
10%
7.8%
5.7% 5%
3.3% 0%
At Discharge
At 1 Month
At 1 Year
V Invasive (n=462)
V Conservative (n=458)
Boden H, N Engl J Med 1998; 339:1091-9

31. Time since start of open-label dalteparin (days)
FRISC II TRIAL
0.16
0.14
0.12
0.10
Probability of death or myocardial infarction
0.08
Non-invasive group
0.06
Invasive group
0.04
0.02 60
120
180
240
300
360
Time since start of open-label dalteparin (days)
Wallentin L, Lancet 2000;356:9-16

32. Considerazioni nei pazienti anziani
Hamm C W et al. Eur Heart J 2011;32:

33. CRUSADE Score: emorragia maggiore intra-ospedaliera

34. Terapia antitrombotica

35. Addressing the Challenge of Selecting an Anticoagulation Strategy
Bleeding Risk
Ischemic Risk
Renal function
Age
Time to cath
Cost
Ease of use
PCI vs CABG vs Med Rx 35

36. Antiplatelet agents: Aspirin
IIa
IIb
III
Aspirin is recommended for all patients presenting with NSTE-ACS without contraindication at an initial loading dose of 160–325 mg (non-enteric), and at a maintenance dose of 75–100 mg long-term. A
Eur Heart J 2007;28:1598–1660 I
IIa
IIb
III
Aspirin should be given to all patients without contraindications at an initial loading dose of 150–300 mg, and at a maintenance dose of 75–100 daily long-term regardless of treatment strategy. A
Hamm C W et al. Eur Heart J 2011;32:

37. Antiplatelet agents: P2Y12 receptor inhibitors
Clopidogrel I
IIa
IIb
III
For all patients, an immediate 300 mg loading dose of clopidogrel is recommended, followed by 75 mg clopidogrel daily. Clopidogrel should be maintained for 12 months unless there is an excessive risk of bleeding A
In patients considered for an invasive procedure/PCI, a loading dose of 600 mg of clopidogrel may be used to achieve more rapid inhibition of platelet function B
Eur Heart J 2007;28:1598–1660
Hamm C W et al. Eur Heart J 2011;32:

38. Study Design, Flow and Compliance
25,087 ACS Patients (UA/NSTEMI 70.8%, STEMI 29.2%)
Planned Early (<24 h) Invasive Management with intended PCI
Ischemic ECG Δ (80.8%) or ↑cardiac biomarker (42%)
Randomized to receive (2 X 2 factorial):
CLOPIDOGREL: Double-dose (600 mg then150 mg/d x 7d then 75 mg/d) vs Standard dose (300 mg then 75 mg/d)
ASA: High Dose ( mg/d) vs Low dose ( mg/d)
Angio 24,769
(99%)
PCI 17,232
(70%)
No PCI 7,855 (30%)
No Sig. CAD 3,616
CABG 1,809
CAD 2,430
Compliance:
Clop in 1st 7d (median) 7d d d d
Efficacy Outcomes: CV Death, MI or stroke at day 30
Stent Thrombosis at day 30
Safety Outcomes: Bleeding (CURRENT defined Major/Severe and TIMI Major)
Key Subgroup: PCI v No PCI
Complete Followup 99.8%
The CURRENT–OASIS 7 Investigators N Engl J Med 2010; 363:

39. Clopidogrel: Double vs. Standard Dose Primary Outcome: PCI Patients
CV Death, MI or Stroke
Clopidogrel Standard
15% RRR
0.04
Clopidogrel Double
0.03
Cumulative Hazard
0.02
HR 0.85
95% CI
P=0.036
0.01
0.0 3 6 9 12 15 18 21 24 27 30
Days
The CURRENT–OASIS 7 Investigators N Engl J Med 2010; 363:

40. Clopidogrel Double vs Standard Dose Bleeding PCI Population
Hazard
Ratio
95% CI P
TIMI Major1
0.5
1.06
0.79
CURRENT Major2
1.1
1.6
1.44
0.006
CURRENT Severe3
0.8
1.39
0.034
Fatal
0.15
0.07
0.47
0.125
ICH
0.035
0.046
1.35
0.69
RBC transfusion ≥ 2U
0.91
1.49
0.007
CABG-related Major
0.1
1.69
0.31
1ICH, Hb drop ≥ 5 g/dL (each unit of RBC transfusion counts as 1 g/dL drop) or fatal
2Severe bleed + disabling or intraocular or requiring transfusion of 2-3 units
3Fatal or ↓Hb ≥ 5 g/dL, sig hypotension + inotropes/surgery, ICH or txn of ≥ 4 units
The CURRENT–OASIS 7 Investigators N Engl J Med 2010; 363:

41. Antiplatelet agents: P2Y12 receptor inhibitors
Prasugrel I
IIa
IIb
III
None
Eur Heart J 2007;28:1598–1660
Hamm C W et al. Eur Heart J 2011;32:

42. TRITON-TIMI 38 Aspirin ACS (STEMI or UA/NSTEMI) and Planned PCI
10,074 with unstable angina or non–ST-elevation myocardial infarction
Aspirin
Double-blind
Prasugrel
60 mg LD, 10 mg/day
Clopidogrel
300 mg LD, 75 mg/day
Median duration of therapy 12 months
1o end point: CV death, MI, stroke
2o end points: CV death, MI, stroke, rehospitalization CV death, MI, UTVR
Stent Thrombosis
Wiviott, SD, et al. N Engl J Med 2007;357:

43. Death from Cardiac Causes, Nonfatal MI, or Nonfatal Stroke
TRITON-TIMI 38:
Primary Endpoint at 15 Months
Death from Cardiac Causes, Nonfatal MI, or Nonfatal Stroke
P<.001
P<.001
% of Patients
P=.31
P=.93
All Kaplan-Meier estimates
Wiviott SD, et al. N Engl J Med. 2007;357(20):

44. TRITON-TIMI 38: Safety at 15 Months
P<.001
% Events
P=.03
P=.23
P=.01
P=.002
p. 2011, Table 3
p. 2007, col 1
ARD = difference between point values (%) *
*Most frequent sites of life-threatening bleeding: Gastrointestinal, intracranial, puncture, and retroperitoneal.
Wiviott SD, et al. N Engl J Med. 2007;357(20):

45. TRITON TIMI 38: CV Death/MI/Stroke Major Subgroups
Reduction in risk (%) 18
10,074 with unstable angina
or non–ST-elevation
myocardial infarction
UA/NSTEMI
STEMI 21
Male 21
Female 12 25
<65
Age
65-74 14
>75 6 14
No DM DM 30 20
BMS
DES 18 21
p. 2010, Fig 2
GPI
No GPI 16 14
CrCl <60
CrCl ≥60 20
Pint=NS
OVERALL 19
0.5 1 2
Clopidogrel better
Prasugrel better
Hazard Ratio
Wiviott SD, et al. N Engl J Med. 2007;357(20):

46. TRITON TIMI 38: REMARKS
Concerns have been raised on the efficacy of Plasugrel in
The elderly
Female gender
Renal insufficiency
The relative antiplatelet effects of prasugrel versus high-dose clopidogrel in percutaneous coronary intervention patients are unknown at least in terms of outcomes
Wiviott SD, et al
The Prasugrel in Comparison to Clopidogrel for Inhibition of Platelet Activation and Aggregation–Thrombolysis in Myocardial Infarction 44 Trial (PRINCIPLE-TIMI 44) Circulation 2007
Overall mortality did not differ significantly between treatment groups. .

47. Antiplatelet agents: P2Y12 receptor inhibitors Ticagrerol
IIa
IIb
III
None
Eur Heart J 2007;28:1598–1660
Hamm C W et al. Eur Heart J 2011;32:

48. PLATO STUDY Primary endpoint: CV death + MI + Stroke
NSTEMI ACS (moderate-to-high risk) STEMI (if primary PCI) (N=18,624)
Clopidogrel-treated or -naive; randomized <24 hours of index event
At randomization, 13,408 (72%) of patients were specified by the Investigator: intent for invasive strategy
Clopidogrel (n=6,676)
If pre-treated, no additional loading dose;
if naive, standard 300 mg loading dose,
then 75 mg qd maintenance;
(additional 300 mg allowed pre-PCI)
Ticagrelor (n=6,732)
180 mg loading dose, then
90 mg bid maintenance;
(additional 90 mg pre-PCI)
6–12 months treatment
Primary endpoint: CV death + MI + Stroke
Primary safety endpoint: Total major bleeding
PCI = percutaneous coronary intervention; CV = cardiovascular; PI = principal investigator
Wallentin L et al.N Engl J Med 2009; 361:

49. Clopidogrel vs. Ticagrelor
Myocardial infarction
Cardiovascular death 8 8
Clopidogrel
6.6 6 6
5.3
Cumulative incidence (%)
Clopidogrel
Ticagrelor
Cumulative incidence (%)
4.3 4 4
3.4
Ticagrelor 2 2
HR 0.80 (95% CI = 0.69–0.92), p=0.002
HR 0.82 (95% CI = 0.68–0.98), p=0.025 60
120
180
240
300
360 60
120
180
240
300
360
Days after randomization
Days after randomization
No. at risk
Ticagrelor
6,732
6,268
6,173
6,010
4,924
3,766
3,078
6,732
6,439
6,375
6,241
5,141
3,591
3,233
Clopidogrel
6,676
6,157
6,062
5,917
4,849
3,706
2,987
6,676
6,376
6,332
6,209
5,114
3,917
3,164
Wallentin L et al.N Engl J Med 2009; 361:

50. Primary efficacy endpoint by clopidogrel loading dose
KM % at Month 12
Hazard Ratio (95% CI)
Total Patients
p value (Interaction)
Characteristic
Ti.
Cl.
HR (95% CI)
Clopidogrel loading dose (Pre-rand. + Study drug)
0.917
300 mg
9314
9.5
11.2
0.85 (0.74, 0.96)
600 mg
4091
8.0
9.5
0.83 (0.67, 1.03)
0.2
0.5
1.0
2.0
Ticagrelor better
Clopidogrel better
Wallentin L et al.N Engl J Med 2009; 361:

51. Primary safety event: Major bleeding*15
Clopidogrel
11.6
Ticagrelor
11.5 10
K-M estimated rate (% per year) 5
HR 0.99 (95% CI = 0.89–1.10), p=0.88 60
120
180
240
300
360
Days after randomization
* PLATO definitions
Wallentin L et al.N Engl J Med 2009; 361:

52. PLATO TRIAL: REMARKS Ticagrelor: unsolved issues
Given that both prasugrel and ticagrelor appear superior to clopidogrel, how would they compare against each other, especially in clopidogrel nonresponders?
The relative antiplatelet effects of prasugrel versus high-dose clopidogrel are unknown at least in terms of outcomes
Gurbel PA, et al The ONSET/OFFSET Study Circulation 2009;120:
In December 2010 the FDA requested additional ASA dose analyses from PLATO which were provided in January Ticagrelor appear to be even more effective if used with
lower dose maintenance ASA. (Results still unpublished). .

53. Glycoprotein IIb/IIIa receptor inhibitors
The choice of combination of oral antiplatelet agents, a GP IIb/IIIa receptor inhibitor, and anticoagulants should be made in relation to the risk of ischemic and bleeding event
Among patients who are already treated with dual (oral) antiplatelet therapy the addition of a a GP IIb/IIIa receptor inhibitor for high-risk PCI (elevated troponin, visible thrombus) is recommended if the risk of bleeding is low
Eptifibatide or tirofiban added to aspirin should be considered prior to angiography in high risk patients not preloaded with P2Y12 inhibitors
In high-risk patients eptifibatide or tirofiban may be considered prior to early angiography in addition to dual (oral) antiplatelet therapy, if there is ongoing ischemia and the risk of bleeding is low.
GP IIb/IIIa receptor inhibitor are not recommended routinely before angiography in an invasive treatment strategy
GP IIb/IIIa receptor inhibitor are not recommended routinely for patients on dual (oral) antiplatelet therapy treated conservately B C C A A
Hamm C W et al. Eur Heart J 2011;32:

54. Study Design – Second Randomization
Moderate-high risk unstable angina or NSTEMI undergoing an invasive strategy (N = 13,800)
Bivalirudin
Alone
UFH or Enoxaparin
Routine upstream GPI in all pts
GPI started in CCL for PCI only R
Routine upstream
GPI in all pts
Deferred GPI
for PCI only
UFH, Enoxaparin,
or Bivalirudin
VS.
Moderate-
high risk
ACS
Primary analysis
Aspirin in all
Clopidogrel
dosing and timing
per local practice
Secondary
analysis
ACUITY Design. Stone GW et al. AHJ 2004;148:764–75

55. Ischemic Composite Endpoint
Upstream IIb/IIIa vs. Selective IIb/IIIa vs. Bivalirudin alone 15
Estimate P
(log rank)
Routine Upstream IIb/IIIa (N=4605)
7.1%
Deferred PCI IIb/IIIa (n=4602)
7.9%
0.14 10
Bivalirudin alone (N=4612)
7.8%
0.28
Cumulative Events (%) 5 5 10 15 20 25 30 35
Days from Randomization

56. Major Bleeding Endpoint
Upstream IIb/IIIa vs. Selective IIb/IIIa vs. Bivalirudin alone 5 10 15 20 25 30 35
Estimate P
(log rank)
Routine Upstream IIb/IIIa (N=4605)
6.1%
Deferred PCI IIb/IIIa (n=4602)
4.9%
0.009
Bivalirudin alone (N=4612)
3.0%
<0.001
Cumulative Events (%)
Days from Randomization

57. Clinical Implications
Much of the evidence supporting the use of glycoprotein IIb/IIIa agents comes from an era prior to routine early invasive management
Given the increased frequency of upstream oral P2Y12 inhibitor use, the upstream use of GP IIb/IIIa inhibitors (in combination with or in place of oral P2Y12 inhibitors) has been questioned because of concerns about excessive bleeding risk.
Further reviews are needed to identify certain subgroups of patients who are likely to derive a net clinical benefit from upstream GP IIb/IIIa inhibitor use in an early invasive strategy

58. Anticoagulation
Hamm C W et al. Eur Heart J 2011;32:

59. Oasis-5

60. Recommendations for anti-ischemic drugs
IIa
IIb
III
Oral or intravenous nitrate treatment is indicated to relieve angina: intravenous nitrate treatment is recommended in patients with recurrent angina and/or signs of heart failure
Patients on chronic Beta-blocker therapy admitted with ACS should be continued on Beta-blocker therapy if not in Killip class ≥III
Oral Beta-blocker treatment is indicated in all patients with LV dysfunction without contraindications
Clacium channel blockers are recommended for symptoms relief in patients receiving nitrates and beta-blockers (dihydropyridines type), and in patients with contraindications to Beta-blocker (benzothaizepine or phenyelthyalamine type)
Calcium channel blockers are recommended in patients with vasospastic angina
Intravenous Beta-blocker treatment at the time of admission should be considered for patients in a stable haemodynamic condition (killip class< III) with hypertension and/or tachycardia
Nifedipine, or the dihydropyridines, are not recommended unless combined with B-blockers B B B C C B
Hamm C W et al. Eur Heart J 2011;32:

61. Decision making algorithm in ACS
Hamm C W et al. Eur Heart J 2011;32:

62. Terapia di prevenzione secondaria
Hamm C W et al. Eur Heart J 2011;32:

63. Complicanze dell’Infarto Acuto del Miocardio
Precoci
Morte improvvisa
Fase acuta
Aritmie
Insufficienza mitralica: necrosi dei muscoli papillari
Scompenso cardiaco
Shock cardiogeno
Giorni successivi
Estensione dell’infarto,
Angina
Embolie polmonari o sistemiche
Complicanze di tipo meccanico
Pericardite epistenocardica
Complicanze post-acute
Aritmie ipercinetiche,
Sindrome di Dressler ( Pericardite di Dressler)
Recidiva di infarto miocardico.

64. Pericardite Epistenocardica
Quasi esclusivamente dopo infarto transmurale
Segno indiretto di gravità del danno miocardico ischemico
Clinica
Ripresa di dolore toracico (terza, quarta giornata, entro i primi sette giorni)
Dolore è sensibile alle variazioni posturali, ai colpi di tosse alle profonde inspirazioni.
10% dei casi sfregamento pericardico
Si può associare:
Versamento pericardico
Febbre
Leucocitosi
VES
ECG
Modifiche della fase di ripolarizzazione ventricolare
Tachicardia sinusale
Aritmie sopraventricolari
Accentuazione del sopraslivellamento del tratto ST (derivazioni diverse da quelle dell’infarto ed a concavità superiore)
Diagnosi differenziale
Estensione dell’infarto
Fenomeni embolici polmonari
Broncopolmonite

65. Sindrome di Dressler Compare da 1-8 settimane dopo l’infarto Clinica
Malessere generale
Febbre
Dolore pericardico
Leucocitosi
↑VES
Versamento pericardico
Causa non definita chiaramente
Riscontro di anticorpi contro il tessuto cardiaco fa pensare ad una genesi autoimmunitaria
Risponde prontamente alla terapia steroidea

66. Pericardite post-infartuale
Trattamento
Antiinfiammatori (aspirina ed indometacina)
Diuretici (riduzione del versamento pericardico se presente)
Corticosteroidi solo in caso di refrattarietà alla terapia con FANS (ritardano il processo di cicatrizzazione → rischio rottura parte ventricolare)