Is troponin Guided thrombolyis an accepted concept ?
Yes , only in few situations like , posterior MI , LBBB , pacemaker rhythm, re infarction .(Note , true posterior MI do not elevate the ST segment but depress it ) .
One may be surprised why we shouldn’t lyse a patient whenever troponin is elevated in acute coronary syndrome (After all it denotes myocardial necrosis and infarct !) The point here is , troponin can raise in all forms of MI (NSTEMI, even in some cases of chronic stable angina ) Read in this link Why thrombolysis is contrindicated in UA/NSTEMI
The benefits of thrombolysis is not proven in small and micro infarcts. ECG ST eelvation remain the sole criteria for thromolysis for STEMI because of high degree of correlation with total coronary occlusion .
In this era of rapid interventions the treatment concepts has blurred as we tend to do PCI and stenting most cases of ACS including UA/Unstable angina
OK , what happened to this patient ?
Temporary pacer was kept stand by with a sheath and catheter in situ.
Next day morning AV block disappeared .Patient was comfortable .
To our surprise , in the same evening his ECG showed a complete heart block with AV dissociation . Still the heart rate was good . The demand temporary pacemaker didn’t take over .
On the third day , every conduction disturbance disappeared and patient was sent to the wards. He is being discharged in a stable condition with std drugs .there was a minimal wall motion defect in infero-posterior segments with an ejection fraction of 50 % . He is scheduled for coronary angiogram 2 weeks later.
What is the pathology ?
Pathologicallyit could be a small focal area of Infarct incidenataly invloving the AV node .(This is alss refered to as vital area Infarct” )It is hard to differentiate whether AV block is due to revrible ischemia or necrosis , simple tissue edema , high vagal tone . or combination of above .If the block recovers it can be concluded necrosis is not the dominant theme.
STEMI presenting primarily as heart block is less common . When such a presentation occurs extra caution is required.
Many of these patients may not show a classical ST elevation and hence do not permit us to thrombolyse as per criteria.
It is the individual physician’s discretion to do so ( or not to do ! ) . No body is going to fault. After all 5 % of thrombolyis world over is for benign early repolarisation syndromes.
The above description is an example of complicated inferior MI . . . still managed effectively by conventional methods.