Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 106

In addition to the classic contraindications, fibrinolysis is contraindicated in a patient with an expected intracranial bleeding risk of >4% (e.g., an elderly [>75] small woman with HTN).²⁰

Consider fibrinolytic therapy successful if: chest pain resolves and initial ST-segment elevation decreases by more than 50% (preferably 70%) at 60–90 minutes after therapy initiation, in the lead showing the worst ST-segment elevation. Also, the occurrence of an accelerated idioventricular rhythm (AIVR) in conjunction with the preceding features is highly specific for reperfusion. In the absence of a response (persistent ischemic symptoms, ST elevation, or both), plan for emergent rescue PCI. It is best to start transferring the patient to a PCI-capable hospital as soon as fibrinolytic therapy is started, so that, if no response is seen at 60 minutes, cardiac catheterization is readily available.

Table 2.1 Limitations and contraindications of fibrinolysis.

LimitationsPatency of the infarct-related artery (TIMI 2 or 3 flow) is achieved in ~75–80%. TIMI 3 flow is achieved in 55–60% aIntracranial hemorrhage: 0.5–1.5%Major bleeding: ~5%Early recurrent ischemia or MI: 10–20% (within hours or days) Most important absolute contraindicationsAny prior intracranial hemorrhageIschemic stroke <3 months. Ischemic stroke >3 months is a relative contraindicationSevere acute hypertension unresponsive to acute therapyActive bleeding (except menses)Cranial or spinal surgery <2 monthsClosed head or facial trauma <1 month, even without a documented bleed (e.g., recent fall with head trauma) Most important relative contraindicationsIschemic stroke >3 monthsSevere acute HTN (SBP >180 or DBP >110) responsive to acute therapyChronic severe hypertensionRecent major surgery or internal bleed <2–4 weeks. Proliferative retinopathy is not a contraindicationOral anticoagulant therapy, including warfarin with INR >2 (strong relative contraindication)

^a Full patency with <50% residual disease is achieved in only 15–20%.

Figure 2.3 Fibrinolysis cascade and mechanism of action of fibrinolytics. Fibrinolytics activate plasminogen into plasmin, which degrades fibrin. PAI-1, plasminogen activator inhibitor (~ tPA inhibitor); r-PA, reteplase; r-tPA, alteplase; TNK, tenecteplase; tPA, tissue plasminogen activator.

A successful fibrinolysis correlates with TIMI 3 flow on coronary angiography. TIMI grade 0 flow implies the absence of any flow. TIMI 1 flow implies the presence of some flow beyond the obstruction but without full distal perfusion. TIMI 2 flow means that the vessel is fully perfused but the flow is slow compared with a normal artery and/or the contrast material clears more slowly than in a normal artery; TIMI 2 flow is related to a residual mechanical obstruction or to microvascular obstruction from microvascular emboli. TIMI 3 flow means full perfusion of the vessel with normal flow. In fibrinolytic trials, TIMI 3 flow has been shown to be associated with the lowest mortality. TIMI 2 flow is associated with an intermediate mortality, while TIMI 0–1 flow is associated with the highest mortality.^22,23 The outcome is improved in patients whose TIMI 2 flow eventually improves to TIMI 3 flow within a few days (this happens two-thirds of the times).²⁴ In a patent artery, TIMI 2 and 3 flow patterns are associated with divergent outcomes and should not be grouped together.

Following PCI and in the absence of any residual mechanical obstruction, the flow may still be TIMI 0–2 flow because of microvascular embolization, spasm, or edema; this is called no reflow, i.e., TIMI 0–2 flow without any residual epicardial stenosis. The term “no reflow” is used only with PCI, not with fibrinolysis.