Re: Carotid IMT Nonatherosclerotic causes

[Guest guest]

Live and learn, " I did not know that " (think ny Carson). Your point is

taken.

However, I was defending the wider idea that heart attacks don't happen in

the absence of underlying pathology and inasmuch as the below mechanisms are

all pathological, the general point is reinforced.

Al

> Nonatherosclerotic causes of coronary artery narrowing--Parts I, II &

> III

>

> Approximately 5% of patients with acute myocardial infarction do

> not have atherosclerotic coronary artery disease but have other

> causes for their luminal narrowing. The first part of this

> three-part review of nonatherosclerotic causes of coronary

> narrowing focuses on congenital coronary artery anomalies,

> coronary fistula, and high take-off position of coronary ostia.

>

> PMID: 8790958

>

> Part II of this three-part article on nonatherosclerotic causes

> of coronary heart disease focuses on myocardial bridges,

> coronary artery aneurysms, emboli, coronary dissection, and

> spasm as causes of luminal narrowing.

>

> PMID: 8818441

>

> Approximately 5% of patients with acute myocardial infarction do

> not have atherosclerotic coronary artery disease but have other

> causes for their luminal narrowing. The third part of this

> three-part review of nonatherosclerotic causes of coronary

> narrowing focuses on coronary vasculitis, infectious diseases,

> Kawasaki's disease, metabolic disorders, metastatic disease, and

> substance abuse (cocaine).

>

> PMID: 8864340

>

>

>

>

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4:51 PM

[Guest guest]

Hi folks:

The question this very interesting post (the one about 5% of heart

attacks being caused by non-athersclerotic constriction of the

coronary artery) seems to raise is: " In cases like this there

presumably isn't plaque that can break off and travel downstream to

block the coronary artery. So in these cases what is the substance

that plugs the already-constricted artery, and what is its origin? "

The 5% number is interesting also. Because I believe in Japan just

6% of deaths are from cardiac causes. Is this the 6% of them who

have non-atherosclerotic arterial anomalies? If so then they have

pretty much zero problems with arteries getting clogged with plaque.

Which presumably says even more about the benefits of japanese

lifestyle for CVD.

Rodney.

>

>

> Live and learn, " I did not know that " (think ny Carson). Your

point is

> taken.

>

> However, I was defending the wider idea that heart attacks don't

happen in

> the absence of underlying pathology and inasmuch as the below

mechanisms are

> all pathological, the general point is reinforced.

>

> Al

>

>

> > Nonatherosclerotic causes of coronary artery narrowing--Parts I,

II &

> > III

> >

> > Approximately 5% of patients with acute myocardial infarction

do

> > not have atherosclerotic coronary artery disease but have other

> > causes for their luminal narrowing. The first part of this

> > three-part review of nonatherosclerotic causes of coronary

> > narrowing focuses on congenital coronary artery anomalies,

> > coronary fistula, and high take-off position of coronary ostia.

> >

> > PMID: 8790958

> >

> > Part II of this three-part article on nonatherosclerotic

causes

> > of coronary heart disease focuses on myocardial bridges,

> > coronary artery aneurysms, emboli, coronary dissection, and

> > spasm as causes of luminal narrowing.

> >

> > PMID: 8818441

> >

> > Approximately 5% of patients with acute myocardial

infarction do

> > not have atherosclerotic coronary artery disease but have

other

> > causes for their luminal narrowing. The third part of this

> > three-part review of nonatherosclerotic causes of coronary

> > narrowing focuses on coronary vasculitis, infectious

diseases,

> > Kawasaki's disease, metabolic disorders, metastatic disease,

and

> > substance abuse (cocaine).

> >

> > PMID: 8864340

> >

> >

> >

> >

>

>

> --------------------------------------------------------------------

------------

>

>

> No virus found in this incoming message.

> Checked by AVG Free Edition.

> Version: 7.5.446 / Virus Database: 268.18.11/721 - Release Date:

3/13/2007

> 4:51 PM

>

[Guest guest]

Hi, Al. That wasn't directed at you - just some general info.

At 81, my father was given the go ahead for post-stroke exercise based

mostly on his good ejection fraction. I was surprised that was about

the only basis for the decision, since he also had ~85% occlusion in a

carotid. I was more surprised that the GP said there was no need to

limit the heart rate. The only warning was to watch for chest pain. It

all worked out well with no problems.

Everybody here would already know (since Ornish) that atherosclerosis

in cardiac arteries might be reversed. But that doesn't happen in a

carotid. However, the carotid blockage can change its character, to

become more solidified, so to speak, and less likely to suddenly

rupture.

I'd also just add that there is such a thing as 'idiopathic

ventricular fibrillation', though that might not come under the

meaning of the phrase 'heart attack'. Also, there is fibrillation due

to mineral imbalance or maybe a drug reaction. Again, that is not a

'heart attack' per se and besides would not result in a stent.

Thursday, March 15, 2007, 10:31:54 AM, Al wrote:

AY> Live and learn, " I did not know that " (think ny Carson). Your point is

AY> taken.

AY> However, I was defending the wider idea that heart attacks don't happen in

AY> the absence of underlying pathology and inasmuch as the below mechanisms are

AY> all pathological, the general point is reinforced.

AY> Al

>> Nonatherosclerotic causes of coronary artery narrowing--Parts I, II &

>> III

>>

>> Approximately 5% of patients with acute myocardial infarction do

>> not have atherosclerotic coronary artery disease but have other

>> causes for their luminal narrowing. The first part of this

>> three-part review of nonatherosclerotic causes of coronary

>> narrowing focuses on congenital coronary artery anomalies,

>> coronary fistula, and high take-off position of coronary ostia.

[Guest guest]

Also:

Sudden cardiac death not related to coronary atherosclerosis.

Ladich E,

Virmani R,

Burke A.

CVPath, International Registry of Pathology, Inc., Gaithersburg, MD 20878, USA.

Sudden cardiac death (SCD) accounts for approximately 300,000 cardiac events in the United States each year, representing an overall incidence of 0.1-0.2% per year. Although the vast majority of these may be attributed to coronary atherosclerosis, a wide variety of nonatherosclerotic-related cardiac diseases have been associated with SCD. This review highlights three general categories of cardiac disease not related to atherosclerosis: the cardiomyopathies, inflammatory myocardial diseases, and ion channel disorders. The important role played by genetics in some of these cardiovascular diseases is presented as well as toxic and drug-related etiologies.

PMID: 16507544

Re: [ ] Carotid IMT Nonatherosclerotic causes

Live and learn, "I did not know that" (think ny Carson). Your point is taken.However, I was defending the wider idea that heart attacks don't happen in the absence of underlying pathology and inasmuch as the below mechanisms are all pathological, the general point is reinforced.Al

..

[Guest guest]

Hi Ken:

Are you sure about this? (Second sentance attached below) If so how

can that be reconciled with:

" Carotid artery IMT was approximately 40% less in the CR group than in

the comparison group. "

(From what has become known here as 'The WUSTL Study': PMID: 15096581)

The CR subjects had not always been restricted. Presumably prior to

their starting CR their carotid IMT had been similar to that of the

control group?

More good news!

Rodney.

> Everybody here would already know (since Ornish) that atherosclerosis

> in cardiac arteries might be reversed. **** But that doesn't happen

> in a carotid ****.

[Guest guest]

I was wondering about that, too. I don't know of an apartheid mechanism

in the arteries whereby some arteries can benefit from a regimen without

the others doing so as well.

Maco

At 12:48 PM 3/15/2007, you wrote:

Hi Ken:

Are you sure about this? (Second sentance attached below) If so how

can that be reconciled with:

" Carotid artery IMT was approximately 40% less in the CR group than

in

the comparison group. "

(From what has become known here as 'The WUSTL Study': PMID:

15096581)

The CR subjects had not always been restricted. Presumably prior to

their starting CR their carotid IMT had been similar to that of the

control group?

More good news!

Rodney.

--- In

, Ken <trails@...>

wrote:

> Everybody here would already know (since Ornish) that

atherosclerosis

> in cardiac arteries might be reversed. **** But that doesn't happen

> in a carotid ****.

[Guest guest]

Here is some data on cardiac deaths:

" Deaths due to cardiovascular disease remain the largest contributor

to premature mortality in most developed societies. Of the 2 400 000

US deaths in 1999, 720 000 (30%) were directly attributed to cardiac

diseases. Of this number, the US Centers for Disease Control and

Prevention estimated that 462 000, or 64% of the subtotal,

were " sudden cardiac deaths " (SCDs), using their definition of SCD as

including all deaths " ...due to cardiac disease that occurred out of

hospital (341 000) or in an emergency department, or one in which the

decedent was reported `dead on arrival' " (page 123).1 Contributing

comorbidities and actual precipitating causes of death are,

unfortunately, not reflected in these data. And, although recorded

as " sudden, " the majority of deaths tabulated in this statistic are

the ultimate result of complex pathologies that develop progressively

over a period of years, encompassing many different clinical and

etiological phenotypes able to influence terminal arrhythmogenesis

through multiple mechanisms. The concept of " sudden arrhythmic death "

(SAD), implying the " sudden " occurrence of fibrillation or a

potentially lethal ventricular tachy- or bradyarrhythmia as a cause

of death, would be a more informative phenotype, but the terminal

arrhythmia is often not documented in the community. One estimate of

the potential magnitude by which ventricular arrhythmias underlie the

SCD problem was provided recently by a study of deaths occurring

within the community at large. Using electrocardiographic data from

first responders alone, Cobb et al2 estimated that 185 000 SADs occur

annually in the US, results similar to the estimate of 250 000

provided by Myerburg et al3 using a somewhat different approach.

Given the prevalence of cardiovascular diseases potentially

associated with lethal ventricular arrhythmia (13 000 000 affected US

individuals),4 approximately 5% of the middle-aged US population has

a presently indeterminable, but significant predisposition to SCD. "

From: http://circres.ahajournals.org/cgi/content/full/94/6/712

Rodney.

[Guest guest]

Hi All,

How about the below paper?

Toyofuku M, Goto Y, Matsumoto T, Miyao Y, Morii I,

Daikoku S, Itoh A, Miyazaki S, Nonogi H.

[Acute myocardial infarction in young Japanese women]

J Cardiol. 1996 Dec;28(6):313-9. Japanese.

PMID: 8986854 http://tinyurl.com/2o6ymy

The fraction of patients of age younger than 50 years

among all age groups was lower in female than in male

acute myocardial infarction patients (5% vs 13%, p <

0.01). The increase of the coronary risk factors,

hypercholesterolemia (25% vs 55%, p < 0.05) and

cigarette smoking (17% vs 96%, p < 0.05) were less

common in women. In female patients, the serum total

cholesterol level was lower (195 +/- 50 vs 216 +/- 48

mg/dl, p = 0.06), and the serum high-density

lipoprotein cholesterol level was higher (50 +/- 12 vs

39 +/- 12 mg/dl, p < 0.05) than in male patients.

Other risk factors did not differ significantly

between the two groups. Angiography 1 month after

myocardial infarction showed fewer diseased coronary

arteries (> 75% stenosis) in female than male patients

(0.8 +/- 0.9 vs 1.8 +/- 1.0, p < 0.01), and normal

coronary arteries were seen in 35% of female patients

(male 6%, p < 0.05). Ten female patients (42%) had

obviously non-atherosclerotic causes of acute

myocardial infarction: Takayasu aortitis in three

patients, coronary embolism in two, acute dissection

of the aorta in two, and idiopathic coronary artery

dissection, Kawasaki disease, and systemic lupus

erythematosus in one each. In contrast, among male

patients, only one had coronary embolism (1%).

In-hospital mortality was higher in women (17%) than

in men (2%, p < 0.05). Young female patients (< 50

years) with acute myocardial infarction have a low

incidence of hyperlipidemia and normal coronary

arteries or involvement of the left main trunk are

more common compared with male patients (< 50 years).

Although 42% of female patients had obvious

non-atherosclerotic etiology of acute myocardial

infarction, the causes varied widely.

--- Rodney <perspect1111@...> wrote:

> Hi folks:

>

> The question this very interesting post (the one

> about 5% of heart

> attacks being caused by non-athersclerotic

> constriction of the

> coronary artery) seems to raise is: " In cases like

> this there

> presumably isn't plaque that can break off and

> travel downstream to

> block the coronary artery. So in these cases what

> is the substance

> that plugs the already-constricted artery, and what

> is its origin? "

>

> The 5% number is interesting also. Because I

> believe in Japan just

> 6% of deaths are from cardiac causes. Is this the

> 6% of them who

> have non-atherosclerotic arterial anomalies? If so

> then they have

> pretty much zero problems with arteries getting

> clogged with plaque.

> Which presumably says even more about the benefits

> of japanese

> lifestyle for CVD.

>

> Rodney.

>

>

> >

> >

> > Live and learn, " I did not know that " (think

> ny Carson). Your

> point is

> > taken.

> >

> > However, I was defending the wider idea that heart

> attacks don't

> happen in

> > the absence of underlying pathology and inasmuch

> as the below

> mechanisms are

> > all pathological, the general point is reinforced.

> >

> > Al

-- Al Pater, PhD; email: Alpater@...

________________________________________________________________________________\

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Expecting? Get great news right away with email Auto-Check.

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[Guest guest]

Thursday, March 15, 2007, 12:05:30 PM, Rodney wrote:

R> The question this very interesting post (the one about 5% of heart

R> attacks being caused by non-athersclerotic constriction of the

R> coronary artery) seems to raise is: " In cases like this there

R> presumably isn't plaque that can break off and travel downstream to

R> block the coronary artery. So in these cases what is the substance

R> that plugs the already-constricted artery, and what is its origin? "

Rodney, I think you're assuming that a clot has to originate in

atherosclerotic plaque. Are you aware of how a single fatty meal can

kill a person (IIRC specifically the fat irritates endothelium into

producing clotting factor VII, fibrinogen, etc).

So if we look for a similar acute result from snow shovelling:

PMID: 14523316

Med Sci Sports Exerc. 2003 Oct Coagulation and fibrinolytic

responses to manual versus automated snow removal.

" Snow shoveling acutely increases fibrinolytic potential in this

population, although not to the degree observed after maximal

treadmill exercise. "

For shovelling, they showed a pro-thrombotic factor increasing, and an

anti-thrombotic factor decreasing. Age would likely figure in.

One group using a snow thrower shows no effect - i.e., it's not the

cold, etc causing pro-thrombotic conditions.

The treadmill group does worst, I would think because the feet are

pounding the floor (think of the platelets in the foot circulation).

The treadmill also increased von Willebrand Factor, another highly

pro-thrombotic substance.

[Guest guest]

Hi Ken:

I don't believe I was assuming anything. I was asking two

questions. To which I think you have provided a partial

answer .... that a coronary artery blockage can be caused by a

blood clot as well as by ruptured plaque.

The origin of the plaque seems pretty obvious. The origin of the

clot appears to be attributed to 'fibrinolysis' whatever that is.

This may be relevant to us because it seems that even if we have no

plaque, our coronary artery might also be blocked by a clot.

So further information on this may be helpful in suggesting ways we

can avoid clot formation.

My impression now is that heart problems may result from:

Plaque rupture.

Electrical malfunction, arrhythmia. (SCD).

Blood clot.

Cardiovascular system structural faults. (Anuerysm .....).

Others?

Rodney.

Ken <trails@...> wrote:

>

> Thursday, March 15, 2007, 12:05:30 PM, Rodney wrote:

>

> R> The question this very interesting post (the one about 5% of

heart

> R> attacks being caused by non-athersclerotic constriction of the

> R> coronary artery) seems to raise is: " In cases like this there

> R> presumably isn't plaque that can break off and travel downstream

to

> R> block the coronary artery. So in these cases what is the

substance

> R> that plugs the already-constricted artery, and what is its

origin? "

>

> Rodney, I think you're assuming that a clot has to originate in

> atherosclerotic plaque. Are you aware of how a single fatty meal can

> kill a person (IIRC specifically the fat irritates endothelium into

> producing clotting factor VII, fibrinogen, etc).

>

> So if we look for a similar acute result from snow shovelling:

>

> PMID: 14523316

>

> Med Sci Sports Exerc. 2003 Oct Coagulation and fibrinolytic

> responses to manual versus automated snow removal.

>

> " Snow shoveling acutely increases fibrinolytic potential in this

> population, although not to the degree observed after maximal

> treadmill exercise. "

>

> For shovelling, they showed a pro-thrombotic factor increasing, and

an

> anti-thrombotic factor decreasing. Age would likely figure in.

>

> One group using a snow thrower shows no effect - i.e., it's not the

> cold, etc causing pro-thrombotic conditions.

>

> The treadmill group does worst, I would think because the feet are

> pounding the floor (think of the platelets in the foot circulation).

> The treadmill also increased von Willebrand Factor, another highly

> pro-thrombotic substance.

>

[Guest guest]

Saturday, March 17, 2007, 12:56:11 AM, Rodney wrote:

R> Hi Ken:

R> I don't believe I was assuming anything. I was asking two

R> questions. To which I think you have provided a partial

R> answer .... that a coronary artery blockage can be caused by a

R> blood clot as well as by ruptured plaque.

R> The origin of the plaque seems pretty obvious. The origin of the

R> clot appears to be attributed to 'fibrinolysis' whatever that is.

I'm glad you mentioned that, Rodney, because I had misstated the

results.

Lysis is to break down, being the opposite of genesis. E.g., you have

lipolysis for fat, glycolysis for glucose, glycogenolysis for

glycogen. So fibrinolysis is the breaking down (dissolving) of clots,

which are built around fibrin. (Fibrinogen leads to fibrin, which is

roughly like threads or strands that interweave with platelets to form

clots.)

R> This may be relevant to us because it seems that even if we have no

R> plaque, our coronary artery might also be blocked by a clot.

yes, when it hits an obstruction - or else just finally travels to a

spot that is normally and naturally so narrow it can't go farther: an

arteriole or capillary.

The snag I hit was when I mentally glossed over the results and had

not pasted: " young, healthy males " . So in that group, shovelling

actually tends toward clot **dissolving**. Mea culpa. Sorry for the

error.

However, the von Willebrand Factor is involved in platelet adhesion to

blood vessel walls, and does lead to coagulation. But the vWF was

increased only in the treadmill group. That might be from the foot

pounding; but we also don't know how hard/fast the snow shovelling

actually was. I myself never had a treadmill stress test, and don't

know how hard that is. So the intensity may or may not be greater than

the shovelling they did.

Here's a related article, which says that studies on older people

would be done:

http://www.scienceblog.com/community/older/2001/A/200110591.html

" Whether the findings apply to older individuals, who are at greater

risk for heart attack, remains to be determined in a follow-up study

the investigators are conducting.

'There is already good data to show that aging reduces the potential

for clot dissolving, " Womack says. " We want to find out whether aging

also affects the response of these parameters during exercise.' "

I'll look for that, after I get done snow shovelling...

R> So further information on this may be helpful in suggesting ways we

R> can avoid clot formation.

Here's a review that I located, about meals and acute clot formation.

which is a related subject:

http://www.bentham.org/cnf/sample/cnf1-1/D0003NF.pdf

R> My impression now is that heart problems may result from:

R> Plaque rupture.

R> Electrical malfunction, arrhythmia. (SCD).

R> Blood clot.

R> Cardiovascular system structural faults. (Anuerysm .....).

R> Others?

R> Rodney.

R> Ken <trails@...> wrote:

>>

>> Thursday, March 15, 2007, 12:05:30 PM, Rodney wrote:

>>

>> R> The question this very interesting post (the one about 5% of

R> heart

>> R> attacks being caused by non-athersclerotic constriction of the

>> R> coronary artery) seems to raise is: " In cases like this there

>> R> presumably isn't plaque that can break off and travel downstream

R> to

>> R> block the coronary artery. So in these cases what is the

R> substance

>> R> that plugs the already-constricted artery, and what is its

R> origin? "

>>

>> Rodney, I think you're assuming that a clot has to originate in

>> atherosclerotic plaque. Are you aware of how a single fatty meal can

>> kill a person (IIRC specifically the fat irritates endothelium into

>> producing clotting factor VII, fibrinogen, etc).

>>

>> So if we look for a similar acute result from snow shovelling:

>>

>> PMID: 14523316

>>

>> Med Sci Sports Exerc. 2003 Oct Coagulation and fibrinolytic

>> responses to manual versus automated snow removal.

>>

>> " Snow shoveling acutely increases fibrinolytic potential in this

>> population, although not to the degree observed after maximal

>> treadmill exercise. "

>>

>> For shovelling, they showed a pro-thrombotic factor increasing, and

R> an

>> anti-thrombotic factor decreasing. Age would likely figure in.

>>

>> One group using a snow thrower shows no effect - i.e., it's not the

>> cold, etc causing pro-thrombotic conditions.

>>

>> The treadmill group does worst, I would think because the feet are

>> pounding the floor (think of the platelets in the foot circulation).

>> The treadmill also increased von Willebrand Factor, another highly

>> pro-thrombotic substance.

>>

[Guest guest]

Saturday, March 17, 2007, 12:56:11 AM, Rodney wrote:

R> So further information on this may be helpful in suggesting ways we

R> can avoid clot formation.

as anti-platelet:

the tried and true daily aspirin, which once you start you have

increased risk if you stop

(then there is Plavix aka clopidogrel, which costs maybe $3-4 per pill

instead of 3 cents for aspirin, and has shown the inevitable serious

side effects once released for general use. Plavix AFAIK has no

meaningful advantage over aspirin for heart, I know it doesn't for

stroke)

for non-drug, the 2 most powerful that I know are fish oil (EPA and

DHA might differ in effect) and then vit E

then also cinnamon, ginkgo, garlic, even cranberry.

R> My impression now is that heart problems may result from:

R> Plaque rupture.

R> Electrical malfunction, arrhythmia. (SCD).

R> Blood clot.

R> Cardiovascular system structural faults. (Anuerysm .....).

R> Others?

valve problems like the famous mitral valve prolapse (these give the

audible murmur, though I've also seen an MD pronounce that a murmur

was present when it was not); and congenital tiny holes, though IIRC

holes usually heal when children grow up; also infection

speaking of aspirin, we know to give two aspirin to a person to chew

when a heart attack is suspected, but NEVER give when a stroke is

suspected

[Guest guest]

Hi folks:

Further to this issue I found the following listing of cardiovascular

diseases on the American Heart Association website:

Atherosclerosis

High blood pressure

Heart attack

Angina

Arrhythmia

Stroke - two types

Congenital defects - various

Rheumatic heart disease

Congestive heart failure - more than one type

'Other', including:

Bacterial endocarditis

Cardiomyopathy

Kawasaki disease

Peripheral vascular diseases

It would be nice if we had incidence and mortality data for these

diseases. There are data on the AHA website but not, as far as I can

make out, broken down as above.

Rodney.

--- In , " Rodney " <perspect1111@...>

wrote:

>

> Here is some data on cardiac deaths:

>

> " Deaths due to cardiovascular disease remain the largest

contributor

> to premature mortality in most developed societies. Of the 2 400

000

> US deaths in 1999, 720 000 (30%) were directly attributed to

cardiac

> diseases. Of this number, the US Centers for Disease Control and

> Prevention estimated that 462 000, or 64% of the subtotal,

> were " sudden cardiac deaths " (SCDs), using their definition of SCD

as

> including all deaths " ...due to cardiac disease that occurred out

of

> hospital (341 000) or in an emergency department, or one in which

the

> decedent was reported `dead on arrival' " (page 123).1 Contributing

> comorbidities and actual precipitating causes of death are,

> unfortunately, not reflected in these data. And, although recorded

> as " sudden, " the majority of deaths tabulated in this statistic are

> the ultimate result of complex pathologies that develop

progressively

> over a period of years, encompassing many different clinical and

> etiological phenotypes able to influence terminal arrhythmogenesis

> through multiple mechanisms. The concept of " sudden arrhythmic

death "

> (SAD), implying the " sudden " occurrence of fibrillation or a

> potentially lethal ventricular tachy- or bradyarrhythmia as a cause

> of death, would be a more informative phenotype, but the terminal

> arrhythmia is often not documented in the community. One estimate

of

> the potential magnitude by which ventricular arrhythmias underlie

the

> SCD problem was provided recently by a study of deaths occurring

> within the community at large. Using electrocardiographic data from

> first responders alone, Cobb et al2 estimated that 185 000 SADs

occur

> annually in the US, results similar to the estimate of 250 000

> provided by Myerburg et al3 using a somewhat different approach.

> Given the prevalence of cardiovascular diseases potentially

> associated with lethal ventricular arrhythmia (13 000 000 affected

US

> individuals),4 approximately 5% of the middle-aged US population

has

> a presently indeterminable, but significant predisposition to SCD. "

>

> From: http://circres.ahajournals.org/cgi/content/full/94/6/712

>

> Rodney.

>