Myocardial Infarction Treatment and Diagnosis

The correct answer is A

Explanation


A working definition for acute evolving myocardial infarction in the presence of clinically appropriate symptoms has been established as


(1) patients with ST-segment elevation, i.e. new ST-segment elevation at the J point with the cut-off points 0.2mV in V1through V3and 0.1mV in other leads, or

(2) patients without ST-segment elevation, i.e. ST-segment depression or T wave abnormalities.

Clinically established myocardial infarction may be defined by any Q wave in leads V1through V3, or Q wave 0.03s in leads I, II, aVL, aVF, V4, V5or V6.


Neither the GISSI-2/International Trials nor the Third International Study of Infarct Survival(ISIS 3)found a difference in mortality between the use of streptokinase and tissue plasminogen activator or anistreplase. Furthermore, the addition of subcutaneous heparin did not reduce mortality compared with the use of no heparin.


However, the GUSTO Trial (Global Utilisation of Streptokinase and Tissue Plasminogen Activator for occluded coronary arteries)28 employed an accelerated t-PA (tissue type plasminogen activator) regimen given over 90min29 rather than the previously conventional period of 3h. Accelerated t-PA with concomitant APTT (activated partial thromboplastin time) adjusted intravenous heparin was reported to result in 10 fewer deaths per 1000 patients treated. The risk of stroke is higher with t-PA or anistreplase than with streptokinase.


In the GUSTO trial, there were three additional strokes per 1000 patients treated with accelerated t-PA and heparin in comparison with streptokinase and subcutaneous heparin, but only one of these survived with a residual deficit. In assessing the net clinical benefit, this must be taken into account with the reduced death rate in the t-PA group. Several variants of t-PA have been studied. Double-bolus r-PA (reteplase) does not offer any advantage over accelerated t-PA except for its ease of administration. Single-bolus weight-adjusted TNK-tPA (tenecteplase) is equivalent to accelerated t-PA for 30-day mortality and associated with a significantly lower rate of non-cerebral bleeds and less need for blood transfusion.


Bolus fibrinolytic therapy may facilitate more rapid treatment in and out of the hospital and reduce the risk of medication errors. The choice of fibrinolytic agent will depend on an individual assessment of risk and benefit, and also on factors such as availability and cost. For late treated patients more fibrin-specific agents may be more effective

Platelet aggregation is only partly inhibited by aspirin and progress has been made with the development of platelet glycoprotein IIb/IIIa inhibitors, which block the final pathway of platelet aggregation. Angiographic trials demonstrated that the combination of GP IIb/IIIa inhibitors with half-dose fibrinolytic and reduced doses of heparin, induces similar or slightly higher TIMI grade 3 flow rates when compared with full-dose fibrinolytic alone and is associated with more complete resolutionof ST-segment elevations, suggesting an improvement in tissue reperfusion. The clinical benefit and safety of these combinations has been tested in two large trials.No reductions in 30-day mortality or intracranial haemorrhage rates but lower rates of in-hospital reinfarction were observed, however, at the cost of an increase in (mostly spontaneous) non-cerebral bleeding complications especially in elderly patients.

Therefore, the routine use of a reduced dose fibrinolytic with abciximab or other platelet glyco-protein IIb/IIIa inhibitors cannotbe recommended. Whether this combination therapy may be beneficial in specific subgroups of patients (for example those at high risk or those likely to undergo early PCI) needs to be further evaluated.

Heparin has been extensively used during and after fibrinolysis, especially with tissue plasminogen activator. Heparin does not improve immediate clot lysis but coronary patency evaluated in the hours or days following thrombolytic therapywith tissue plasminogen activator appears to be better with intravenous heparin. No difference in patency was apparent in patients treated with either subcutaneous or intravenous heparin and streptokinase.Prolonged intravenous heparin administration has not been shown to prevent reocclusion after angiographically proven successful coronary fibrinolysis. Heparin infusion after tissue plasminogen activator therapy may be discontinued after 24–48h. Close monitoring of intravenous heparin therapy is mandatory; aPTT values over 70s are associated with higher likelihood of mortality, bleeding and reinfarction. Although no randomized trials have beenperformed, there is evidence from recent trials suggesting that more frequent monitoring of aPTT and a full weight adjustment of heparinmay decrease the risk of non-cerebral bleeding complications.

http://eurheartj.oxfordjournals.org/cgi/content/full/24/1/28

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