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Heart Disease (Expert Forum)
A-FIB, LVOT Obstruction due to SAM
This forum is for questions and support regarding heart issues such as: Angina, Angioplasty, Arrhythmia, Bypass Surgery, Cardiomyopathy, Coronary Artery Disease, Defibrillator, Heart Attack, Heart Disease, High Blood Pressure, Mitral Valve, Pacemaker, PAD, Stenosis, Stress Tests
A-FIB, LVOT Obstruction due to SAM
by LacyMary, Jul 10, 2005 12:00AM
I am grateful I was able to get thru. Thank You.
Had several Echo's in the past. All Normal except mild Mitral/Aortic Regurgitation and one time, showed, "positive stress echo for apical-septal ischemia".
Had new Echo 2 weeks after "1st attack of A-FIB" which Corvert IV,converted to NSR in 10 min. All Enzymes normal, in ER.
Glucose144, HCT was 55(H) Potassium 3.5(L), Chloride 112(H) Creatinine (L) RDW (L)
5 hours later, Troponim was 4.85 and CK-MB, elevated. These numbers came down hourly until discharged. They do not have a clue what caused the A-FIB or the rise in Troponin, CK-MB, 5 hours later. Cath only showed a 60% blockage and was stented.
Echo after this "heart Event" showed "30mmHg Dynamic LVOT OBstruction due to SAM". EF was 58%
Question: What exactly is a 30mmHg Dynamic LVOT due to SAM? Since other previous Echo's were normal, could there be a relation between this new Echo finding and the A-FIB attack, 2 weeks earlier? I am looking for a reason for the A-FIB attack. Dehydrated? (been on Avalide 150/12.5 for months) Plavix also, TopolXL and Crestor.
2.I had a heart cath last December. 2 stents placed in RCA due to "pressure readings" being 68. What does low pressure mean?
3. What are your thoughts on a Cardiac MRI showing things a Cath will not pick up? Would this be good to clarify the last Echo findings and looking for the cause/damages from the A-FIB attack since there was a rise of Heart Enzymes 4 hours after the "heart Event".
Being CC is No. One for Cardiac Care, I look forward to your expertise reply. Thanks.
Lacy,55.
Had several Echo's in the past. All Normal except mild Mitral/Aortic Regurgitation and one time, showed, "positive stress echo for apical-septal ischemia".
Had new Echo 2 weeks after "1st attack of A-FIB" which Corvert IV,converted to NSR in 10 min. All Enzymes normal, in ER.
Glucose144, HCT was 55(H) Potassium 3.5(L), Chloride 112(H) Creatinine (L) RDW (L)
5 hours later, Troponim was 4.85 and CK-MB, elevated. These numbers came down hourly until discharged. They do not have a clue what caused the A-FIB or the rise in Troponin, CK-MB, 5 hours later. Cath only showed a 60% blockage and was stented.
Echo after this "heart Event" showed "30mmHg Dynamic LVOT OBstruction due to SAM". EF was 58%
Question: What exactly is a 30mmHg Dynamic LVOT due to SAM? Since other previous Echo's were normal, could there be a relation between this new Echo finding and the A-FIB attack, 2 weeks earlier? I am looking for a reason for the A-FIB attack. Dehydrated? (been on Avalide 150/12.5 for months) Plavix also, TopolXL and Crestor.
2.I had a heart cath last December. 2 stents placed in RCA due to "pressure readings" being 68. What does low pressure mean?
3. What are your thoughts on a Cardiac MRI showing things a Cath will not pick up? Would this be good to clarify the last Echo findings and looking for the cause/damages from the A-FIB attack since there was a rise of Heart Enzymes 4 hours after the "heart Event".
Being CC is No. One for Cardiac Care, I look forward to your expertise reply. Thanks.
Lacy,55.
Doctor's Answer
by CCF-M.D.-MJM, Jul 10, 2005 12:00AM
Hi Lacy,
I am sorry to hear abour your recent health problems.
1. What exactly is a 30mmHg Dynamic LVOT due to SAM? Since other previous Echo's were normal, could there be a relation between this new Echo finding and the A-FIB attack, 2 weeks earlier? I am looking for a reason for the A-FIB attack. Dehydrated? (been on Avalide 150/12.5 for months) Plavix also, TopolXL and Crestor.
There are many causes of dynamic outflow tract obstruction. What it means is the the anterior (front) leaflet of your mitral valve is partially obstructing the outflow tract of your heart (the blood going into your systemic circulation). When we see this it is important to real out a disease called hypertrophic cardiomyopathy -- although it is caused by several other conditions. People with SAM tend to have increased left ventricular pressures which translates into increased atrial pressures and therefore can lead to atrial fibrillation. People with think heart muscle (hypertrophy) or hypertrophic cardiomyopathy sometimes don't tolerate A fib very well and occassionally have enzyme leaks (elevated troponin and CK MB).
At the Cleveland Clinic Dr. Lever and Dr. Thamalarison specialize in this disease. If you are any where near Cleveland consider getting a second opinion from them (I don't mean to advertise but they are very good). You will see their names mentioned on this forum occassionally.
2.I had a heart cath last December. 2 stents placed in RCA due to "pressure readings" being 68. What does low pressure mean?
I am not 100% sure what they are referring to. It may be a pressure wire that measures the pressure proximal and distal to the obstruction to determine its clinical (physiologic) significance.
3. What are your thoughts on a Cardiac MRI showing things a Cath will not pick up? Would this be good to clarify the last Echo findings and looking for the cause/damages from the A-FIB attack since there was a rise of Heart Enzymes 4 hours after the "heart Event".
I do not think an MRI will clarify this question. Consider getting a second opinion and look for someone that specialized in hypertrophic cardiomyopathy.
As an important side note, if we see some with a resting gradient and SAM we give an inhalant called amyl nitrite to reduce system pressure and look for an increase in the gradient. In some patients the pressures do not change but others increase dramatically and may help identify people at more risk for symptoms and problems related to the obstruction. Dehydration will likely increase the gradient as well.
I hope this helps. Good luck.
I am sorry to hear abour your recent health problems.
1. What exactly is a 30mmHg Dynamic LVOT due to SAM? Since other previous Echo's were normal, could there be a relation between this new Echo finding and the A-FIB attack, 2 weeks earlier? I am looking for a reason for the A-FIB attack. Dehydrated? (been on Avalide 150/12.5 for months) Plavix also, TopolXL and Crestor.
There are many causes of dynamic outflow tract obstruction. What it means is the the anterior (front) leaflet of your mitral valve is partially obstructing the outflow tract of your heart (the blood going into your systemic circulation). When we see this it is important to real out a disease called hypertrophic cardiomyopathy -- although it is caused by several other conditions. People with SAM tend to have increased left ventricular pressures which translates into increased atrial pressures and therefore can lead to atrial fibrillation. People with think heart muscle (hypertrophy) or hypertrophic cardiomyopathy sometimes don't tolerate A fib very well and occassionally have enzyme leaks (elevated troponin and CK MB).
At the Cleveland Clinic Dr. Lever and Dr. Thamalarison specialize in this disease. If you are any where near Cleveland consider getting a second opinion from them (I don't mean to advertise but they are very good). You will see their names mentioned on this forum occassionally.
2.I had a heart cath last December. 2 stents placed in RCA due to "pressure readings" being 68. What does low pressure mean?
I am not 100% sure what they are referring to. It may be a pressure wire that measures the pressure proximal and distal to the obstruction to determine its clinical (physiologic) significance.
3. What are your thoughts on a Cardiac MRI showing things a Cath will not pick up? Would this be good to clarify the last Echo findings and looking for the cause/damages from the A-FIB attack since there was a rise of Heart Enzymes 4 hours after the "heart Event".
I do not think an MRI will clarify this question. Consider getting a second opinion and look for someone that specialized in hypertrophic cardiomyopathy.
As an important side note, if we see some with a resting gradient and SAM we give an inhalant called amyl nitrite to reduce system pressure and look for an increase in the gradient. In some patients the pressures do not change but others increase dramatically and may help identify people at more risk for symptoms and problems related to the obstruction. Dehydration will likely increase the gradient as well.
I hope this helps. Good luck.
Just wanted to add my two cents about Dr. Thalmilarasan. He is a fabulous and very caring physican!! I am not familiar with the other physician mentioned, but if he is anything like Dr. T...you can't go wrong.
Good luck and hope you are feelinb better!
Connie
But, there is a nagging feeling in the back of my mind that I do!. Something is not right. I cannot get my pulse under 90 and it will shoot up in a matter of seconds to 130 for no reason and then I get weak and disoriented. I have printed this out for the Heart Center Doctors here. I need closure to all of this and yes, CC is on my insurance plan.
I am on Maxide now and NorpaceCR but not doing well on these.
Thank you very much, Doctor and Mom.
Is this conditon helped with surgery? I want it gone NOW! (-: Thanks again.
Mom3, what did you see Dr. T for? I l1ve about 1500 miles from Cleveland Clinic but willing to travel if I know I will get well. Thanks again, nice people. God Bless.
Remember, I want to make sure I didn't lead you to believe you have HCM, just that when we see SAM we make sure that isn't HCM.
Good luck.
My best to you, doctor.
My best to you, doctor.
I was referred to CC when I developed cardiomyopathy (EF 40%). Because I have mitral regurgitation, the immediate thought was that the leaky valve was the culprit. My EP is associated with another Cleveland hospital and is an expert in her field, but she said CC is the BEST place for a valve repair/replacement.
After a thorough examination, Dr. Lauer (CC) scheduled me for a TEE. Anyway, Dr. Shiota and Dr. Thalmilarasan performed and monitored the TEE. They were wonderful!! Dr. T. is an expert echocardiographer and he was involved in reviewing my prior echo (I brought it with me) as well as the TEE.
Anyway, turned out that the cardiomyopathy was not a result of the leaky valve. With this new information, my EP consulted with several echocardiographers (in Cleveland and around the country) and the consensus was that the CM was very possibly the result of my persistent pvcs. Because it is so rare, I posted a question to one of the doctors on this forum regarding any studies about cardiomyopathy and persistent pvcs.
To make a very long story short, the forum doctor (based on what I wrote and the limited information he had) was very concerned and wanted to be sure I was not being misled. He was worried that the valve was indeed the problem. So, I phoned my EP and explained the forum doctor's concerns. She explained why she felt my CM was NOT because of the valve, but rather b/c of the pvcs. So, I decided to call Dr. T b/c he read the actual reports and performed the TEE. He returned my call and very willingly, accepted my offer to phone my EP. THEN, he called me back in the evening and discussed my doctor's evaluations, etc. and confirmed that although it is RARE, it made a lot of sense and seemed quite reasonable. Turns out my EP was right b/c since my ablations in 2003, my EF has gone up at each exam and it is finally back to 60% and I'm feeling SO much better. YEAH!
I'm sure that's more than you wanted to know (LOL), but I wanted you to know just how nice he was. No doubt, if I need further valve studies, I will not hesitate to schedule an appt. with Dr. T!! He is so compassionate and friendly! He told me to call ANYTIME if I had questions!! I can't say enought good things about his professionalism and very kind bedside manner. Good luck!! Feel better soon!!
connie
I personally feel that my problems stemmed from elevated BP for a long time that no one would treat. It is was Labile...(good and bad)or some genetic condition. Dad died suddenly at the age of 39.
I am on Norpace that the EP doctor wants me on in case I have another A-Fib Attack and also back on TopolXL 50mg. Plus now separate Maxide and Avapro plus Plavix. I feel I should be on a Blood