Week 4 - Alex

This week, I started shadowing Dr. Ip. I met with him on Monday afternoon, and discussed my plan for shadowing and working on one of his research projects. 

This summer, I will be working with him on a clinical research project to understand the effects of adenosine treatment on premature ventricular contractions (PVCs). Premature ventricular contractions are a common arrhythmia that occurs when the ventricles of the heart beat before the normal systolic stimulation. PVCs result in reduced cardiac output on the following systolic beat, as the left ventricular pressure is too low. While PVCs are a common, and non-lethal arrhythmia, some people with PVCs will have a reduced overall cardiac output, as the ratio of PVCs to systolic ventricular contraction can approach one in four.

Adenosine is a drug that is effective at reducing the rate of PVCs in a subset of the population. However, it’s not understood why some people respond to the treatment, while others do not. The focus of Dr. Ip’s research is to use ECG’s to characterize the differences between the two populations. Unfortunately, the data collection has not been completed, but should be in a couple of weeks. I should receive the data in a couple of weeks.

For most of the week, I observed cardiac ablation procedures. Cardiac ablation procedures are performed on patients with a variety of arrhythmias and usually cannot be treated with drugs or an implantable device, alone.

A typical patient who undergoes an ablation procedure will:

1. Arrive at the clinic with an arrhythmia (atrial fibrillation, flutter, ventricular tachycardia, etc).
2. If the patient is not responsive to drug or cardioversion treatment, and their quality of life is significantly affected, a cardiologist or electrophysiologist may recommend an ablation procedure – usually in a few weeks.
3. During the procedure:
1. Many patients who had an arrhythmia in the clinic may resolve it before reaching the EP lab. As a result, the EPs will use drugs and pacing protocols to induce the arrhythmia. 
2. The EP will study the ECGs, and often create a 3D map of the heart to determine where the arrhythmia originates from.
3. The 3D map may include a measure of the tissue’s conductivity (atrial fibrillation), or the activation time of tissue, relative to some temporal marker during an arrhythmic waveform.
4. Using these tools, among others, the EPs are able to localize arrhythmogenic areas, and kill the conductive tissue using an ablation catheter.
5. When a patient’s arrhythmia breaks, the EP tries to re-induce the arrhythmia using drugs and pacing protocols. If they can reinduce it, then they’ll continue ablating other areas.

The above explanation is general: not all cases need a 3D map; not all arrhythmias need inducing; sometimes the EP knows exactly where to ablate without any in-procedure diagnostic data.

While I saw many procedures over the last week, the most exciting was my first. The EP ablated a patient with atrial flutter. The treatment is a simple ablation line in a known region of the right atria. The patient went from atrial flutter to a normal sinus rhythm in an instant. It was amazing.

Next week will include more procedures, and possibly some data analysis for the clinical research project.