Chronicle of My Husband's Heart Attack

The morning of Wednesday, January 9, 2008, at about 9 AM Jim was taken to the Catheterization Lab at Boston Medical Center. He underwent a cardiac/heart catheterization. Before the cardiologist started this procedure he told Jim’s Dad and I that he was doing the catheterization based on the troponin enzyme levels that rose during the hours after Jim’s heart attack. The cardiologist told us that it usually took 1 hour for him to do the catheterization. If he didn’t find any problems in Jim’s heart, then that would end the procedure. If he did find a problem/blockage, then it usually took him another hour to correct the problem. Jim was sedated but conscious throughout the procedure.

The surgeon found that one of Jim’s three major coronary arteries (the LAD or left anterior descending artery) was 90% blocked. The other two coronary arteries were not blocked. What had happened is that the plaque in Jim’s coronary artery had cracked for some, as yet, unknown reason. Most of us adults in western civilization are walking around with the level of plaque that Jim has. But Jim’s problem is that his plaque cracked. When that happened the platelets, that we all have in our blood, got caught on the tear and formed a clot. That clot is what blocked Jim’s coronary artery. I think that the doctor told us that the recurring periods of chest pressure that Jim felt was his body breaking down the clot and then the clot reforming. This illustration describes plaque that cracks as vulnerable plaque:

A clot that forms at the site of the plaque is called "soft" plaque on the inside of the artery, because the plaque can crack and bleed. This plaque, which has a thin covering over it, is called vulnerable plaque.When vulnerable plaque ruptures, it can cause a blood clot to form. The clot can block the blood flow to the section of heart muscle fed by the artery.

To correct blockage the cardiologist inserted a metal stent in Jim’s blocked coronary artery after he managed to remove the clot (they aren’t always able to remove the clot and it is positively significant that they were able to remove this clot). The surgeon noted that Jim’s artery has a large diameter, and consequently the stent in his artery is relatively large (4.0mm diameter), which is in Jim’s favor as large stents do not get blocked again as easily.

Here is what the Jim’s Discharge Summary states about the procedure:

Patient was admitted and brought to the cath lab on 1/9/2008 (transferred at 23:30 PM 1/8/08). Diagnostic cath revealed nl LM, thrombotic (blood clot) 90% proximal (nearest) LAD (left anterior descending coronary artery-see illustration below), nl Lcx (left circumflex artery) and nl dominant RCA (right coronary artery). He subsequently underwent successful LAD bare metal stent PCI (Percutaneous revascularization using coronary stents or PCI-stenting) with a single 4.0x15mm Vision stent without complications. His right SFA arteriotomy was sealed with an Angioseal closure device and the femoral vein sheath was manually dc’d without complication.

The diagnosis of Jim’s heart episode is officially, Acute Coronary Syndrome:

An acute coronary syndrome (ACS) is a set of signs and symptoms, usually a combination of chest pain and other features, interpreted as being the result of abruptly decreased blood flow to the heart (cardiac ischemia); the most common cause for this is the disruption of atherosclerotic plaque in an epicardial coronary artery.

This is an illustration that shows the location of the LAD (left anterior descending artery) that was 90% blocked in Jim’s heart:

Here is a video describing a cardiac catheterization with stenting (at about the 3:52 point in the video):

vadkins

After experiencing incapacitating pressure in his chest, a to 911 with an ambulance ride to the hospital, Jim was admitted to the nearby hospital in Massachusetts. At the hospital he was seen by a cardiologist who noted that although his EKG was normal, his Troponin blood enzyme levels had risen slightly in the first few hours since the heart episode that morning. Although Jim and I had never heard of Troponin before, we were about to find out all kinds of things about this highly, highly significant (to cardiology) enzyme. From Wikipedia:

Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators of damage to the heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction (heart attack) in patients with chest pain. A patient who had suffered from a myocardial infarction would have an area of damaged heart muscle and so would have elevated cardiac troponin levels in the blood.

Jim’s troponin levels continued to rise during the 6 hours after the heart episode. This was crucial to the correct treatment and management of the medical treatment given to Jim. Remember, that his EKG was normal. Most likely, 20 years ago Jim would have been released from the hospital without the treatment he desperately needed-because only in the last few years has troponin been measured during the hours after a likely heart attack.

Reason for Admission/Chief Complaint from the Discharge Summary:

56 year old man with no significant PMH (past medical history) who was transferred to BMC (Boston Medical Center) from Caritas Christi Norwood Hospital for cardiac catheterization. Patient reports being in usual state of health until the morning of admission (01/08/08) when shortly after eating breakfast he developed a feeling of "fullness" in his esophagus. He has had this in the past and has attributed it to heartburn and mild swallowing difficulties. The difference this time was that the sx’s recurred. Over the ensuing 1 1/2 hours he experienced 4-5 episodes of discomfort associated with nausea, diaphoresis (excessive sweating commonly associated with shock and other medical emergency conditions) and generalized upper body weakness in a crescendo pattern. He was noted by his co-workers to be acutely pale and diaphoretic and 911 was called. Episodes lasted approximately 15 minutes. He felt better lying down, was given Ntg (nitroglycerin) spray x2 and ASA by EMT’s with minimal relief and transported to Caritas Christi Norwood Hospital. He became pain free, EKG demonstrated ST elevation in lead III and the R/I for NSTEMI (Non-ST-Elevation Myocardial Infarction) with CK (also known as CPK) 297 MB 22.6 and troponin 3.4.

At the hospital Jim was put on an IV and given a blood thinner (heparin), aspirin, and blood pressure lowing medications.  Jim was not permitted to  even stand upright after he was admitted to the hospital.

Here is the EKG results for Jim on 1/8/2008:

Normal sinus rhythm with sinus arrhythmia (Wikipedia: Sinus arrhythmia is the mild acceleration followed by slowing of the normal rhythm that occurs with breathing)
Normal ECG
No previous ECGs available
786.50 ICD-9 Code for normals and any codes not available in MUSE (I think that this is a standard to compare medical test results with)

vadkins