Sunday, May 17, 2015

Pacemaker's lead Active versus passive fixation

Pacing leads must be secured in the inside of the heart. Ventricular leads often use passive-fixation mechanisms, such as fins or tines, which lodge in the trabeculae lining the interior of the ventricle. The fins or tines snag the lead into position, and over time, fibrosis grows over the interface between lead and tissue such that the lead is firmly in place in the heart. In fact, chronic leads are so securely fixated by fibrosis that they can be difficult to extract if that is ever necessary.

 Atrial leads typically use active-fixation mechanisms because the interior of the atria tends to be smooth walled and possesses no trabeculae. Of course, active-fixation leads can also be used in the ventricles, if the implanting physician chooses. An active-fixation lead has a corkscrew or helix or another mechanism that is deployed and twisted or screwed into the heart. There are a number of active-fixation leads on the market and most usually involve a small tool to twist or turn to deploy the active-fixation mechanism. These leads are securely fixated right at implant and can be easier to remove, if necessary. Implanting physicians may have ideas as to where they want the leads to be fixated, such as the right ventricular outflow tract, but finding the optimal lead location can involve some trial and error. Once a lead is secured in the heart, it has to be tested to be sure that the electrical characteristics are acceptable. A lead can be properly placed mechanically but yield suboptimal electrical results. In such cases, the physician moves the lead to a new spot and tests it again. It is not at all unusual during implant for a physician to move the leads a few times to achieve the desired electrical performance.

Sunday, May 10, 2015

ECG and information about intracoronary occlusion vs. flowing state and What does the Thrombus color matter ?

Answer to the ECG case challenge !
What is your mind about this strip's timing and expected culprit lesion artery and pathology ? 

We remember  the phases of infarction  :

1- Hyperacute phase :( early injury phase (30 minutes to 6 hours)  :The early phase of infarction is characterised by tall peaked T waves (or hyperacute T waves) and you may also see ST elevation during this phase. This is the end of the thrombolysis window. ST elevation occurs as the injured myocardium repolarises earlier than the healthy tissue. The vector or current of injury is directed away from the injured tissue, towards healthy tissue. ST elevation lasts a variable period of time but usually begins to evolve within the first 24hrs.
2-     Evolving phase (6hrs to 24hrs):
The evolving phase is said to occur when the combined patterns of infarction, injury and ischaemia are present. This is typified by the presence of marked ST segment elevation, Q wave development and later on T wave inversion. This typically occurs over a period of hours to days .
3-    Phase of resolution (24hrs to weeks and months later):
The phase of resolution occurs over a period of days to weeks and even months and is typically characterised by the return of the ST segment and T waves to normal. However the presence of the pathological Q waves is permanent. T wave inversion may still be present until weeks after infarction has occurred, but may persist for months after infarction.
When you have as such first strip's sign of ST segment is getting resolution  and T wave are getting deep and broken and there is no any q wave in precordial leads   , it can be meant that there is flowing vessel and the occlusion is not 100% and once we can estimate it is about 99% which there is somewhat flow of culprit lesion , then we go to the next step which angiography to evaluate our discussion .

Here we are with 99% thrombus containing mid LAD lesion , which confirming our pre-angiographic guesses , now we can see the RCA too. 
In ECG we have minimally elevated ST-segment in inferior lead which confirmed by ECG , but because the RCA is non-dominant and thus not supplying the large area of myocardium and left system is dominant as well and main culprit , we started the PTCA of LAD first . 
This was our thrombus which separated through saline washing , it is white thrombus with tiny fibrin strands !
What does  the thrombus color matter ? 

Venous thrombosis has been traditionally associated with red blood cell and fibrin-rich “red clot,” whereas arterial thrombi superimposed on atherosclerotic lesions are rich in platelets,

giving the appearance of “white clot.” This simple but somewhat dogmatic concept has had important therapeutic implications: “red clot” has been traditionally treated with heparin and

warfarin, while platelet inhibition has been utilized for acute coronary syndromes caused by “white clot.” However, careful morphological analysis of thrombi formed in veins reveals

tangled pale strands of aggregated platelets and fibrin within the mass of red blood cells.

Experimentally induced venous throm- bus in the presence of radiolabeled platelets shows early platelet accumulation at the “head” of the venous thrombus.As the thrombi age, acquisition of platelets slows and the clots become“red,” predominantly composed of fibrin and erythrocytes.

Message !
The traditional staging of ECG and experienced eye as well as it's translation into daily practice will help us to determine the intracoronary status before invasive procedures  and thrombus aspiration is not beneficial in the term of survival but can help us to determine the exact timing of infarction and the exact pathology information.