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Spontaneous Coronary Artery Dissection

WomenHeart
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**Originally posted by user katy 06/20/2005 : 22:29:37 **

Ten years ago, when I was 38, I had a heart attack. I was told it was a spontaneous coronary artery dissection(LAD). I had angioplasty and have had no problems since, but doctors don't know why it happened or if it will happen again. I had no history of heart disease or had any risk factors. I currently take a 81 mg. aspirin everyday. Is there anyone who has had this happen to them, or has any information on this subject?

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47 replies

laurahc

It IS a big help finding other women who've gone through the same thing, isn't it? I felt that same sense of relief when I stumbled upon the WomenHeart community for the first time. :)

A couple of weeks after I got out of the hospital, they sent me for scans of my renal and carotid arteries, and those scans were fine. I don't have the typical physical appearance of someone with Marfan syndrome, for example, and since the peripheral artery scans were normal, they've pretty much ruled out connective tissue disorders.

I have that same fear of it happening again, but I remind myself that SCADs are sort of like lightning strikes, and the odds of being hit by lightning twice are really low. :)

spared

Hi Laura, Have you been to any other specialist? I am going tomorrow to rule out a connective tissue disorder. I wish I knew what caused this. Also, my fear is that it will happen again. The cardiologist says it won't. But.....I still have that worry.

It is so nice knowing that there are others out there that have gone through what I have.

laurahc

Hi spared, I'm 41 and had a heart attack and SCAD on March 30th of this year. No risk factors, no family history, and like you, the doctor was sure I hadn't had a heart attack--until the second round of blood work came back. They did a heart cath the next day and ended up putting in six stents in my right coronary artery; at first it just showed a small tear, but then as they watched, it started coming apart more and more.

I'm glad you're in cardiac rehab--I am too, and it's a great confidence builder.

-Laura

spared

I am 43 years old and 7 weeks ago I had a heart attack after running 4 miles. At first I was in denial but Ifinally after an hour I went to the ER. The doctor was sure that it wasn't a heart attack but then my blood work showed otherwise. I had a heart cath that showed a 90% blockage. They couldn't get the stint through and so they did a by pass. I am still in a bit of shock with all that I have been through. The cardiac surgeon said my arteries are clear and that it was SCAD. I live with a constant fear that it could happen again. I am recovering...but it has been the hardest thing I have ever had to go through. I am so blessed to have a great support network. But, it is wonderful to read about other women who have gone through the same thing. I am in cardiac rehab and that is helping. Also, I started taking lexapro and that has helped with some of the anxiety.

NZGirl

Hi there Helen,
Wow.
I thought that comment deserved a line all of its own, what an amazing story, your virtually spontaneous healing sounds almost as rare as the SCAD itself.
Welcome to the site where you are one of a surprisingly large number of "SCAD patients who have lived" ! Maybe you have already done this, but if you type in SCAD or 'Spontaneous Coronary Artery Dissection' in the 'Find It' box you will find many of our stories. The stories vary in detail of course, but have emotional themes in common which connect us all to each other.
You and I had our SCAD events in the same year ('06), and now I am at the point like you where I also "live each day to the fullest and pray that it will never happen again". You have done so very well to give up smoking, and it's good to see you justifiably celebrating your fantastic weight loss. It sounds like you have not only recovered, but have also given yourself the best chance of a long life. Take Care, Sharon XXX

Helen63

Hello,
I would like to share my story. I will try to keep it short.

In Sept of 06 on a wed morning I got up and had plans to go hot tubing before heading to work.. ( I was in pretty good health a bit overweight but not obese 5'6" about 185 and I did smoke)I was on my way to the hot tub and started to feel a bit of nausea.. I thought "hmmm maybe I better eat something?" I stopped and got a coffee and a few doughnut holes. When I got to the hot tub the nausea had increased quite a bit ..after being in the tub about 1 hour I flew to the bathroom and started vomiting violently for at least 15 minutes...now the pain was coming from the upper chest right between my breasts. I got dressed and went into work..I was in the Pharmacy for about 1/2 hour and ended up in the bathroom vomiting again..I was sitting on the floor at work and my pharmacist said to call my doc (we thought maybe the stomach flu or something) I drove myself about 15 miles to my doctors office and by this time I was crawling into the office feeling like I was giving birth to "Alien" through my chest..they put the EKG on me and all hell broke loose my PA says to me "you are having a heart attack of some kind" I was like "What the hell are you talking about" ended up at local hospital via ambulance 10-15 people pulling and poking at me I was starting to freak out) someone said Cath-lab to me and I started to have a anxiety attack (I have been a State Cert Pharm Tech for 9 yrs bow) so I knew what they were talking about ..I had to force them to give me versed because I was flipping out...when I came back to the cardiologist said to me "I have to send you to the Heart Center at Spectrum Health because I do not know what to do with you ...You have what is call "Spontaneous coronary artery dissection aka SCAD( my right coronary artery was twisting and ripping, inner was ripped, middle was in process of twisting ) he said we must hurry because if middle finishes twisting and proceeds to rip you will die" I was totally stunned and in shock because I still had no idea why. I was place in ICU at Fred and Lena Meijer Heart Center here in Grand Rapids MI ..I became a freak show to all of West Michigan Heart. No one had ever experience a SCAD patient that lived..They were pumping blood thinners through my IV and the blood was flowing right back out at the site of the Heart Cath..(what a mess) for 6 days I was a special guest in ICU ...they went back in through the Cath on the 6th day with intention of placing a Stint but to their total shock ..IT WAS TOTALLY GONE...healed without a trace....Now they really had no idea what to do with me..I was a freak (LOL)..
After extensive research into my medical, mental, and life history they came to the best conclusion they could...Years and years of suppressed stress and anxiety from a 20 year marriage of mostly "hell" (divorced now 4 years) and keeping it from everyone by wearing this "mask" of a perfect marriage and sticking my head in the sand...my body could no longer take it...They say "Stress can Kill" they mean it....
I now no longer smoke and most importantly I no longer allow anyone to walk all over me and I say what I feel when I have to and I have lost 55LBS (YEAHH ME!!) ....I have had a few moments of some high anxiety and ended up back in ER but there were no signs of it happening .....so I live each day to the fullest I can and pray it will never happen again...
Thank you for listening and if anyone has any insight or ideas on this please let me know
HUGS
Helen

NZGirl

Hi titi4,
I can't imagine what it must be like to be told that you have 'paper-thin' veins, it must be very scary, particularly since they have no idea exactly what it is, so therefore I guess no idea how to try and treat it? I hope they do have you on some kind of medication which will lessen the likelihood of further trouble, and I hope your wait isn't too long before they can give you some definitive answers.
What you are dealing with is huge, but I think it proves without a doubt that you and your much-wanted and loved son are meant to be here!
It's reassuring to know that you feel the same as me emotionally, thanks so much for sharing that with me it means more than you could know.
Take Care, Sharon

titi4

Hi NZ Girl,

Thank you for your summary of causes. I fall into 2 of the categories you posted...Post-Partum and Autoimmune Disorder. I had my SCAD a week after my son was born and after genectic testing it was found I have a connective tissue disorder. Pregnancy and such a disorder are fatal, but I obviously not aware. (He was the product of 8 fertility treatments) There are actually 3 top autoimmune disorders that they look for...Marfans, Ehlers Danlos and Loeys-Deitz. Would you believe I fall into "other". There is a 4th and they have not located the gene yet. So my blood awaits with many others. The disorder weakens all arteries and mine were found to be "paper thin". Take that with huge doses of pregnancy hormones and you have a life changing dissection. But I'm still alive!!!!

I am glad you found this site and I emotionally feel exactly like you do. With all the SCAD survivors found here, I often think we should start the 1st SCAD Foundation with our own website!

Be well!
Christine

NZGirl

My understanding of what they believe are the causes of SCAD fall into mostly three categories:
1) Post or Peri-Partum - which seems to involve some kind of hormonal influence (due to the pregnancy) on the arteries
2) Heavy Drug Users - Cocaine etc. The use of heavy drugs apparently causes damage to the arteries and makes them more likely to dissect. (When my doctor asked me about my drug use I told him my drug of choice was Chocolate, and to my knowledge did me no harm except maybe an ever-so-slight link to the way my thighs look......)
3) Idiopathic Group - meaning they have no idea what caused the dissection. This group is the smallest group in terms of numbers and percentages, and this is the group I have been told I fall into. That is because I have always had slightly low blood pressure, have never smoked, my BMI is within the average range, and my total cholesterol is only 3 point something (despite the chocolate...!)
There is another very small group which involves being checked for autoimmune disorders and there are two syndromes they check for, one is Marfans but I can't remember what the other is. One aspect of these disorders apparently makes it more common for arteries to become inflamed and irritated.
Now I get most of my information from the internet, and I am certainly and absolutely no 'expert' so please feel free to pull this apart, it is just what I have gleaned from reading lots of articles about SCAD on the Internet and at the library.
I like the percentages for the two and a half year survival rates, my anniversary for that will be in June this year so perhaps I can let out another breath then.
Take heaps of Care all of you
NZ Girl

titi4

Hello Scad Sisters,

I had found an article on SCAD and it reported that our survival rate increases to 80% 2 1/2 years post dissection. It does not state what our survival rate is until then. My 2 1/2 years anniversary will be 5/2010. Like everyone here, I to am "waiting"....but I will continue to worry the rest of my life.

Annie7

I was not post-partum. I am menopausal.
The ER doctors and the 'holier than thou doc' thought it was my thyroid or that I was an alcoholic (never even had a glass of wine) or I was on street drugs. Gads. There was one cardio fellow from Japan and this doctor was on the ball. He kept mentioning Hyperthropic Obstructive Cardiomyopathy but was downplayed by a cardio in the group. I would follow this Japanese doctor anywhere. He was truly a physician that we all dream of having on our side. I later found out we went back to Japan to practice. He was sooo up with women and heart disease. Perhaps if we all shared a bit more we can perhaps put another piece of the puzzle to this. Thanks NZ Girl. Pls. keep sharing. I wish you the best.

KAKLeon

A question ... as a cardiologist, can you give us a percentage of postpartum versus non-pregnancy related SCAD in the patients you've seen?

Every doctor I've talked with in the last 6 years claims that SCAD is only seen postpartum, yet clearly many of the dissections reported on the message board are not pregnancy related.

Thank you for your interest in SCAD.
Katherine

NZGirl

Hi there Annie7,
Well my understanding of being Paranoid is that it is to be overly worried about things which are not likely to happen - I don't think any of us can be called paranoid, this has happened to us and really could happen again. It must be frightening and frustrating to have the professionals withhold important information from you, and it makes no sense, we need to know exactly what is happening to us when our very lives are at risk.
I am very lucky to have a great doctor and cardiologist, who have answered all of the questions they CAN answer. It's the answers they don't have that worry me.
I just wish that there was more known about the condition so that I could have some reassurance. Just what exactly is 'recovery' in the case of sponataneous dissection? Does it mean you have recovered when you are off your meds, or when you haven't had an 'incident' for a certain period of time? Or are we in limbo? I have read that people do recover completely from heart attacks - since that is so, is there complete recovery for people like us when what caused our heart attack is inexplicable (SCAD) and noone really knows what the future holds?
I hope your new docs continue to keep you well informed, they need to know that this alone can make the difference between a stressed and a relaxed patient. Take Heaps of Care

Annie7

NZGirl, I can relate. I too am waiting. Waiting for what? My last sudden and scary episode was classed as a Heart Event with no MI. (2006) Yet, my Troponin was 4.9 and CK-MB was high. Go figure. I was in A-fib and Tach, I was told at the heart institute. I was shocked back into Normal rythem (sp) and then felt like a million dollars. I wanted to go home but they were waiting for the second set of enzymes to come back (first set was normal) Second set were elevated so I was admitted. It took them 36 hours later to do a heart cath as the cath doctor did not feel it was an Emergency and he had to go someplace. Looking back this should of been done within 6 hours of enzyme elevations. He told my husband that I did not have a heart attack but a heart event. He placed a stent in the mid LAD next to a stent that was placed, a year earlier. The distal LAD is now scarred and too narrow to stent. I did get the report and the Cath CD and this report indicated SDisection. Now I know what this means. He never mentioned this to us. (he was a cocky, self centered, egotisical (sp) doctor that had a Harem of RN's walking behind him) From that incident, I developed a LVOT Obstruction due to Systolic Anterior Motion with a gradient that weaves between 20-30. No one can put a handle on this as to why this happened. I personally feel doctors do not tell all and we should be told everything. I was placed on A-Fib meds which I could not tolerate. I left the group and found doctors closer and a bit more wiser and more forthcoming with information. But, I am still waiting for this repeat most scary episode to happen again. Call me Ms. Paronoid. I wish you well.
Annie

NZGirl

Hi,
I am brand new to this site, but had a heart attack two years ago (Dec 2006) at the age of 43 which was found to be caused by SCAD of the LAD artery.
Ever since then I have been searching for someone who has gone through the same experience, but have found noone. I have read all of the posts about SCAD on this site, and it is just so wonderful to read the experiences of people who have been through this. I feel for you all, it's really scary, and it changes your life.
I had two stents fitted back in Dec 2006, and have been taken back to hospital twice since then for abnormal rhythm problems. Because of that I am still on four different daily medications, but I am keeping quite well.
But after very nearly dying from a very sudden and unexpected event, I am definitely different to who I was before it. Does anyone else feel as if you are 'waiting'. Waiting for what I don't know, but I don't feel as safe as I used to. And since all my doctor and cardiologist can tell me is that this is a very rare event, and so not much is known about it, it leaves you feeling alone with what's inside your head. I have two young sons (they are now eight and ten, they were six and eight when it happened) and I guess I just wish that somehow I could know that this is not going to happen to me again. Wow, a crazy wish I know, but there, I've said it. I want what I can't have, a guarantee that I can go on and live my life without this threat hanging over my head.
Well I have waffled enough for a new member. Sending huge best wishes and kind regards from New Zealand to all of you very courageous people. XXXXX

Kansasdoc

I am a cardiologist. I see spontaneous dissection about once every other year. It is very rare and has to be considered. I have treated patients with angioplasty/stent placement as well as CABG. There is no standard of care because it is so very rare.

nancygrace

Characteristics and Prognosis of Myocardial Infarction in Patients With Normal Coronary Arteries

Peter Ammann, MD; Sabine Marschall, MD; Martin Kraus, MD; Lucius Schmid, MD; Walter Angehrn, MD; Reto Krapf, MD and Hans Rickli, MD
CHEST 117(2):333-338, 2000. © 2000 American College of Chest Physicians

Abstract and Introduction
Abstract
Study objectives: Myocardial infarction with angiographically normal coronary arteries (MINC) is a life-threatening event with many open questions for physicians and patients. There are little data concerning the prognosis for patients with MINC.
Design: Retrospective follow-up study.
Setting: Tertiary referral center.
Patients: Patients with MINC were investigated and compared to age- and sex-matched control subjects with myocardial infarction due to coronary artery disease (CAD). The patients were examined clinically using stress exercise and hyperventilation tests. Migraine and Raynaud’s symptoms were determined by means of a standardized questionnaire. Serum lipoproteins; the seroprevalence of cytomegalovirus, Helicobacter pylori, and Chlamydia pneumoniae infections; and the most frequent causes of thrombophilia were assessed.
Measurements and results: From > 4,300 angiographies that were performed between 1989 and 1996, 21 patients with MINC were identified. The mean ± SD patient age at the time of myocardial infarction was 42 ± 7.5 years. When compared to control subjects (n = 21), patients with MINC had fewer risk factors for CAD. In contrast, MINC patients had more frequent febrile reactions prior to myocardial infarction (six patients vs zero patients; p 4,300 diagnostic coronary arteriographies were performed and 2,100 patients had suffered a prior myocardial infarction. Twenty-five patients (1.2%) with normal coronary arteries and regional hypoakinesia were identified. Twenty-three of them had a classical history of myocardial infarction, definite ECG changes, and a diagnostic increase (greater than twofold) in myocardial enzyme activity. In a second review of the angiograms, done independently by two cardiologists, all of them had angiographically normal coronary arteries without any evidence of endoluminal irregularity. Two patients could not be included in the study because one died in an accident and the other left the country. In our catheter laboratory registry, we identified an age- and sex-matched control group with prior myocardial infarction due to CAD and comparable regional wall motion abnormality. Concerning the seroprevalence studies, a third group of 21 age- and sex-matched healthy blood donors was investigated.
Clinical Investigations
After reviewing the medical records of hospitalization due to myocardial infarction, all patients gave their informed consent for the study. They were asked about angina pectoris before and after the infarction; repeat hospitalizations due to chest pain; new coronary angiographies, or other interventions; febrile infections shortly before infarction; risk factors for CAD (smoking, arterial hypertension, hypercholesterolemia, positive family history, and diabetes mellitus); cocaine abuse; use of sympathomimetics; hormonal contraception; body mass index (BMI); fitness for work; and current medication. Migraine and Raynaud’s symptoms were evaluated by means of a standardized questionnaire in which neither condition was mentioned by name (Table 1). A scoring system was established with points assigned for affirmative responses. Migraine was arbitrarily diagnosed if the score totaled>= 7, and Raynaud’s phenomenon was diagnosed if the score totaled>=4.[11] Calcium channel blockers and lipid lowering medications were discontinued at least 2 weeks before examination in the control group, and all medication was discontinued in patients with MINC (but not the oral anticoagulation in patients with anterior infarction or poor left ventricular function). In order to provoke vasospasm, we performed a test where the patients hyperventilated for 5 min (until the arterial pH was > 7.6) and ECG was continuously monitored for 15 min on a 12-lead ECG (Megacart R/E; Siemens; Solna, Sweden) for ST-segment changes. Patients were asked about chest pain after hyperventilation. After a recovery time of 20 min, a symptom-limited exercise test on a bicycle ergometer (Ergometer 840; Siemens) was performed with stepwise rise in load every 2 min from 25 to 50 W, depending on expected work capacity. ECG and BP were monitored continuously.

Venous blood samples were collected for assessment of thrombophilia, lipid metabolism, and seroprevalence for H pylori, C pneumoniae, and CMV. H pylori-specific IgG titers were measured using a commercial enzyme-linked immunosorbent assay (Cobas Core Anti-H. pylori EIA Art. 07 3497 7; Roche Diagnostics; Rotkreuz, Switzerland). The recommended cutoff point was 6 IU/mL.C pneumoniae IgG and IgA titers were measured using microimmunofluorescence (Chlamydia IgG and IgA SeroFIA No. 511–01E and 513–01E; Savyon Diagnostics; Ashdad, Israel). Cross-reactions with Chlamydia trachomatis and Chlamydia psittaci were assessed. IgG titers >= 1:256 and IgA titers >= 1:64 were considered as positive. Tests for CMV IgG antibodies were performed using an enzyme-linked immunosorbent assay (Cobas Core CMV IgG EIA Art. 07 3494 2; Roche Diagnostics) and considered positive when >= 1.0 U/mL.

Statistics
Values are expressed as frequencies and means ± SD. Group comparisons were made using an unpaired Student’s t test or Mann Whitney U statistic. A p value of 0.05 was considered statistically significant.

Results
The characteristics of the 21 patients available for further study and those of the control group are shown in Table 2. The groups were well matched for age, gender, incidence of anterior infarction, and left ventricular ejection fraction. Twenty-three of 2,100 patients (1.1%) by our definition had MINC. The median time interval between myocardial infarction and coronary angiography was 32 days (range, 8 to 145 days) in the MINC group and 27 days (range, 5 to 261 days) in the CAD group.
In MINC patients, angina pectoris before myocardial infarction was less frequent (1.0 vs 0.7; p = 0.05), and febrile infections, mainly of the upper airways up to 2 weeks prior to infarction, were more frequent (6.0 vs 0.0; p 0.05). MINC patients less frequently had a history of hypercholesterolemia (9 vs 18; p 0.01) and hypertension (2 vs 9; p = 0.05), but there was no significant difference concerning other risk factors, such as family history, hormonal substitution, and diabetes.

Patients with MINC had a significantly lower BMI, whereas BP was similar, probably because of drug treatment. In addition, their migraine score was significantly higher. Furthermore, triglycerides, the cholesterol/high-density lipoprotein (HDL) ratio, and apolipoprotein B were all significantly lower, and HDLs and apolipoprotein A1 were higher in patients with MINC. There were no significant differences in lipoprotein(a) and low-density lipoproteins(Table 2) .

The hematologic variables associated with a thrombophilic state were assessed in 18 of 21 patients (3 patients had to be excluded because of oral anticoagulation). Three MINC patients showed coagulopathy (one with combined protein S/plasminogen deficiency, one with anticardiolipin antibody syndrome, and one with a plasminogen deficiency). Overall, no statistically significant differences in the hematologic variables were found (Table 3). Antibody titers for CMV, H pylori, and C pneumoniae, and immunfluorescence showed no significant difference between MINC and CAD patients. In contrast, when compared to 21 age- and sex-matched healthy blood donors, the prevalence of antibodies against CMV, C pneumoniae, and H pylori was higher in MINC and CAD patients (Table 4).

No ECG or clinical evidence for coronary spasm was provoked in either group by hyperventilation.

Follow-up patients with CAD had a higher incidence of rehospitalization because of angina pectoris (11 vs 0; p 0.0001) and repeated coronary angiography (9 vs 0; p = 0.001) in the follow-up period of at least 7 years (Table 5).

Discussion
One to 12% of individuals with myocardial infarction who undergo coronary angiography are found to have angiographically normal coronary arteries.[5] This wide range can be explained by differing definitions of angiographically normal arteries: "without any endoluminal irregularity" and "no significant stenosis (eg, stenosis 30%)."[16] We defined MINC patients as having no detectable endoluminal irregularities. Using this restrictive definition, 1.1% of patients with myocardial infarction fell into this category. Ten of 21 patients in the MINC group and 11 of 21 patients in the CAD group received fibrinolytic therapy. The long duration between the onset of symptoms and hospitalization was the most common exclusion criteria for fibrinolytic therapy. In the 11 patients of the MINC group without fibrinolytic therapy, spontaneous reperfusion of the infarct-related vessel must be postulated. In patients with CAD, the patency rate of the infarct-related vessel was 73% with and 40% without fibrinolytic therapy. The relatively long duration between myocardial infarction and coronary angiography is explained by delayed referral from other hospitals or preceding cardiac rehabilitation after infarction in some patients.
It is recognized that angiography is not the ideal technique to exclude relevant coronary artery wall changes. However, to our knowledge, there are no studies that have investigated MINC patients by means of intravascular ultrasound, which might show wall changes before they become visible on coronary angiography.

Most previous studies of MINC patients have shown that the typical patient is young, without any previous history of chest pain.[5,9] The mean age of our patients at the time of myocardial infarction was 42 years, with a high percentage of women (40%); this is similar to the largest series of MINC patients, where the mean age was 43 years and 43% were women.[9] Likewise, MINC patients in our study also had significantly less frequent angina prior to myocardial infarction.

Most studies of MINC patients have shown that their cardiovascular risk profile is lower than that of patients with CAD,[9,17] whereas others did not find a difference.[18] We found statistically significant lower BMI, a lower ratio of cholesterol/HDL levels, and a lower incidence of arterial hypertension in MINC patients compared to patients with CAD. In contrast, we found no difference in smoking or therapeutic hormone replacement.

An endothelial dysfunction with a tendency toward increased vasomotor tone has also been implicated.[19] The high migraine score in MINC patients in this and other studies[9] indicates a possible pathophysiologic link. However, when using hyperventilation, it was neither possible to show myocardial ischemia in the 12-lead ECG nor to provoke typical chest pain. Testing with ergonovine maleate might be a superior method to provoke artery spasm in this group of patients.[9]

The fact that smokers show a decreased production of nitric oxide,[20] which partly mediates endothelium-dependent vasodilation, and because most of the patients with MINC are smokers, a pathophysiologic link may seem plausible.[21,22,23,24] However, 76% of our MINC patients and 67% of our CAD patients were smokers at time of infarction. Thus, this factor alone is not a major discriminator between both groups. Cocaine abuse has been shown to cause myocardial infarction in some patients with normal coronary arteries.[25,26] None of our patients reported cocaine abuse prior to myocardial infarction, but analysis of cocaine in urine samples was performed in one patient only.

Three out of 21 patients (16.6%) had biochemical evidence of increased thrombogenicity. This is in contrast to other reports.[18,27] The number of patients tested is too small to generally recommend extensive laboratory screening in these patients.

An interesting finding in our study was the significantly higher number of patients with febrile infections mainly of the upper airways, within 2 weeks prior to infarction in the MINC group. This finding raises new questions of etiology in some MINC patients. Is there a coronary thrombosis and/or a rupture of an angiographically overworked plaque triggered by systemic inflammation itself or by specific infective components? Recent studies have suggested a possible association of C pneumoniae, CMV, and H pylori infections in the etiology of acute coronary syndromes in patients with CAD. Endothelial injury due to circulating endotoxin, autoimmunity with cross-reactivity of bacterial antigens and endothelial cells are discussed as possible underlying mechanisms.[15] Our finding of higher incidence of IgA titers against C pneumoniae as compared to healthy blood donors would be compatible with an inflammatory component of acute myocardial infarction. In this context, it is furthermore tempting to speculate that the higher incidence of febrile infections in our MINC patients might be causally related to their coronary event. However, we found no difference in antibody titers to CMV and H pylori between MINC and CAD patients. Nevertheless, no repeat titer determinations were done and a potential difference with regard to infections with these agents cannot be dismissed.

The febrile episodes before infarction in our MINC patients raise the question as to whether myocarditis might have mimicked acute myocardial infarction in some patients. Myocardial infarction was diagnosed in our patients with MINC by definite ECG changes, a diagnostic increase in myocardial enzyme activity, and, most importantly, regional wall motion abnormality on ventriculography.

The prognosis for MINC patients is excellent. During follow-up at a mean of 5.3 years after infarction, MINC patients had a very good exercise capacity. No one had a major adverse cardiac event or required repeat coronary angiography.

Footnotes

nancygrace

Hi Karen and other scad survivors,

I think your question about whether meds are for dissection or spasm prevention is a good one. It seems most heart meds are for conditions other than spasm or dissection and we scad and spasm people have otherwise healthy arteries or hearts-just something mysterious going on. So what are the meds for? Not cholesterol, not high blood pressure, not clotting (?)

I gradually tapered off my meds (now 6 mo post dissection) due to side effects and the seeming uncertainty and confusion around about just what they were for (and seeing a top cardiologist does not necessarily resolve that confusion b/c scad is rare, thus not much studied, thus remains mysterious condition) and even being told that it is difficult to prescribe accurately b/c something for spasm could aggravate a potential dissection (or vice versa?) .


I do know that a person with history of dissection should not receive lysis in emergency room, which may often be started in emgcy room for MI patients who may be having a thrombosis in the arteries.

If your artery disects and bleeds out, then wouldn't a blood thinner aggravate that if you had another dissection. In other words wouldn't the natural ability of our blood to clot slow down the pooling of blood outside the artery- though I realize clotting could also occude the blood flow through the artery as well. but if the artery is dissected/ or spasming? What will coumadin or plavix do? Or norvasc? I do realize plavix is supposed to protect in case ot late stent thrombosis, but that itself isr elatively rare among stent patients as well.

So in my mind there is a potentially risky situation going (if another dissection could occur or a spasm leading to dissection?) whether using meds or not. The norvasc was giving me plapiations, at least I suspected it was, and in going off it the chronic flutters stopped almost completey. The coumadin/plavix were making my periods extended by another week over normal. Plus my legs felt as if all bruised from the inside which made my walk/jog exercise very uncomfortable. I do not have high blood pressure (though was having transient somewhat high blood pressure sometime before my dissection-which I am trying to figure out) . And I did not have blood clots or plaques.

So I feel more back to normal (and my normal was a fairly active healthy lifestyle) without the meds. I just take aspirin, fish oil (and eat lots of omega 3) and multi vitamin. I also resumed eating my daily spinach and veggie salads and the other veggies I love like broccoli that I was told were giving me too much vit K (while on coumadin). I also happen to like grapefruit , and grapefruit juice and cranberry juice which I was told were not good with coumadin. I also added a small glassof wine daily to my diet . So my diet is better without the meds, and my exercise is easier(on my legs which were hurting-maybe internal bruising or bleeding?)

I don't know if other scad patients feell ok after the dissection, but I do, so do not want all the meds. iIdo wonder if exhaustion that some scad patients mention could be from meds, or from an underlying condition predisposing(autoimmine?) that is undiagnosed. Hormone changes can trigger autoimmuner flares as well. I do have lupus in my family, and have had raynauds (in remission for many years) myself (though I still have the constant cold feeling in my extremities and generally very sensitive to cold) . But autoimmune conditions can flare and remit, so in a flare (which can be aggravated by stress, and MI is very stressful b/c scary) one might be feling exhausted.

I know i'm just throwing out random stuff, but at this point have been thinking of my scad as something that was a fluke or part of a transient flare up or unusual reaction, now remitted. So if I try to stay healthy, reduce stress, andwatch symptoms (I did ignore or fail to recognize symptoms before) maybe it will not be an issue again.

Has anyone else heard of this condition ("MINC") to me it is encouraging:

http://www.medscape.com/viewarticle/405942_4

(I will post text of article in next reply)

nancy grace

TonyaJ

I had GBS during my pregnancies but had my dissection a year ago when our youngest was 8 years old...

Odia

Spontaneous Coronary Artery Dissection is very rare, but about a third of the woman with this diagnosis are in their peripartum or postpartum period. The Drs try to find the connection between the cases. One of the speculations is that It's connected to hormones, but no one knows how the hormones really contribute to this state. Maybe we could find another connection... I know that about 30% of pragnant women have GBS, but as known so far, It can be dangerous only for the baby, If the mother doesn't get antibiotics during delivery. I wondered If, anyhow, there could be any connection to the dissection. Anyhow, I had a postpartum SCAD 5 weeks ago, and ihad GBS in the pregnancy. If other women with SCAD also had GBS, It might be interesting...

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