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Why is my doctor unconcerned with my dilated heart and other abnormalities?
Yesterday I had an appointment with an electrophysiologist whom I'd been referred to by a general cardiologist. I have a history of severe, chronic lightheadedness, with a few faints (one in 2011, another in 2017), and waves of scary-feeling palpitations. The cardiac MRI I took in Jan 2018 showed dilation of all four chambers. The diameter of all four chambers was abnormal, as was the volume in each chamber. I do not have heart failure, because my systolic function is completely normal. I have an EF of 61%, FS of 33%, and a resting stroke volume of 123mL. The MRI showed no late gandolinium enhancement, normal rest perfusion, and no regional or global wall motion abnormalities. I have a massive exercise capacity, as I run about 60 miles a week at roughly 7 flat mile pace, and can race a 5k in the 17 minute range. So, my heart seems to be functioning quite well, and is free of fibrosis and ischemic issues, but I still believe there are concerning issues.
Yet, the electrophysiologist was unconcerned. He said that echos and MRI's are essentially useless, highly variable, subjective estimates. He said that the technology used to measure chamber size and volume is very imprecise, and furthermore that there is much variation on a month to month, year to year basis, and that different technicians would all get different numbers when measuring from the same images. In other words, that any echo/MRI value is just an imprecise estimate, that the actual values would be quite different over time, and that ten different people measuring the same echo/MRI would get ten different results. Thus, he said there's no point in trying to compare my 2018 numbers to the 2012 numbers, and that the numbers on this 2018 MRI may or may not even be accurate, but that even if they were, that's probably just "my normal," and given my normal systolic function the degree of dilation and volume overload I have is not indicative of any pathological process.
I find a lot of this difficult to accept. The degree of variation between my 2012 and 2018 numbers seems far too large to be due to mere normal undulating variation in the values and/or differences in how two different technicians measure. The degree to which values are outside of the normal range seems far too great to merely be "normal for me," rather than the start of some disease process. The fact that my symptoms are now worse, and other findings seem to suggest cardiac dysfunction (pericardial effusion, valve regurgitation, prolonged sinus pauses, documented arrhythmias, etc) is further suspicious to me. Anyways, I'm going to list below my the pieces of evidence that are concerning to me. I appreciate any feedback as to whether or not I should continue to pursue this, as all this guy gave me was a prescription for motion sickness pads and no further referrals to other doctors, nor for further testing.
CONCERNING PIECES OF EVIDENCE
1.) My cardiac MRI in 2018 is far different from my echo in 2012 when I was experiencing severe palpitations. Back in 2012 there was no chamber dilation and the volumes were all normal. So, it appears remodeling has taken place.
2.) I have prolonged sinus pauses on my Holter monitors. They've caught 5 separate pauses of 3-5s on the two Holter's I've worn, which suggests some sort of electrical problem, a problem with the SA node, or a problem with autonomic nervous system.
3.) The MRI revealed mild pericardial and pleural effusions, which seem to suggest that there is some sort of fluid overload beginning to take place.
4.) On my EKG's my QTc interval is usually in the 450-460ms range, which would seem to predispose me to afterdepolarizations that could trigger problematic arrhythmias
5.) My Holter picked up a PVC couplet, which suggests that beyond enhanced automacitity triggering single premature beats there is some sort of structural or functional barrier that enabled reentry, even if only for that one extra beat.
6.) An echo in 2012 showed a prolonged mitral valve deceleration time, possibly suggestive of impaired LV relaxation
7.) My recent MRI showed tricuspid and pulmonary regurgitation, which might suggest the beginning of functional deterioration.
8.) My LV wall and the intraventricular septum have both thinned/stretched out since 2012, going from 1.1cm each to 0.5cm each, suggesting that the dilation remodeling is possibly causing the LV to weaken and/or strain.
9.) I was recently found to have an enlarged liver (I had abdominal pain and elevated enzymes so they took an ultrasound), which can happen when cardiac dysfunction is present.
10.) I've had a chronic cough for the past few years that might correspond with the effusions which may be indicative of cardiac dysfunction
11.) I have other various signs of poor circulation that have developed over the past few years, such as slow healing minor cuts that leave scars, an inability to get an erection, frequent nocturnal urination, etc.
Yet, the electrophysiologist was unconcerned. He said that echos and MRI's are essentially useless, highly variable, subjective estimates. He said that the technology used to measure chamber size and volume is very imprecise, and furthermore that there is much variation on a month to month, year to year basis, and that different technicians would all get different numbers when measuring from the same images. In other words, that any echo/MRI value is just an imprecise estimate, that the actual values would be quite different over time, and that ten different people measuring the same echo/MRI would get ten different results. Thus, he said there's no point in trying to compare my 2018 numbers to the 2012 numbers, and that the numbers on this 2018 MRI may or may not even be accurate, but that even if they were, that's probably just "my normal," and given my normal systolic function the degree of dilation and volume overload I have is not indicative of any pathological process.
I find a lot of this difficult to accept. The degree of variation between my 2012 and 2018 numbers seems far too large to be due to mere normal undulating variation in the values and/or differences in how two different technicians measure. The degree to which values are outside of the normal range seems far too great to merely be "normal for me," rather than the start of some disease process. The fact that my symptoms are now worse, and other findings seem to suggest cardiac dysfunction (pericardial effusion, valve regurgitation, prolonged sinus pauses, documented arrhythmias, etc) is further suspicious to me. Anyways, I'm going to list below my the pieces of evidence that are concerning to me. I appreciate any feedback as to whether or not I should continue to pursue this, as all this guy gave me was a prescription for motion sickness pads and no further referrals to other doctors, nor for further testing.
CONCERNING PIECES OF EVIDENCE
1.) My cardiac MRI in 2018 is far different from my echo in 2012 when I was experiencing severe palpitations. Back in 2012 there was no chamber dilation and the volumes were all normal. So, it appears remodeling has taken place.
2.) I have prolonged sinus pauses on my Holter monitors. They've caught 5 separate pauses of 3-5s on the two Holter's I've worn, which suggests some sort of electrical problem, a problem with the SA node, or a problem with autonomic nervous system.
3.) The MRI revealed mild pericardial and pleural effusions, which seem to suggest that there is some sort of fluid overload beginning to take place.
4.) On my EKG's my QTc interval is usually in the 450-460ms range, which would seem to predispose me to afterdepolarizations that could trigger problematic arrhythmias
5.) My Holter picked up a PVC couplet, which suggests that beyond enhanced automacitity triggering single premature beats there is some sort of structural or functional barrier that enabled reentry, even if only for that one extra beat.
6.) An echo in 2012 showed a prolonged mitral valve deceleration time, possibly suggestive of impaired LV relaxation
7.) My recent MRI showed tricuspid and pulmonary regurgitation, which might suggest the beginning of functional deterioration.
8.) My LV wall and the intraventricular septum have both thinned/stretched out since 2012, going from 1.1cm each to 0.5cm each, suggesting that the dilation remodeling is possibly causing the LV to weaken and/or strain.
9.) I was recently found to have an enlarged liver (I had abdominal pain and elevated enzymes so they took an ultrasound), which can happen when cardiac dysfunction is present.
10.) I've had a chronic cough for the past few years that might correspond with the effusions which may be indicative of cardiac dysfunction
11.) I have other various signs of poor circulation that have developed over the past few years, such as slow healing minor cuts that leave scars, an inability to get an erection, frequent nocturnal urination, etc.
Don't know if it helps but I asked some experts about your case as well. I'll pm you the response.
6. Addressed earlier, diastolic function needs the FULL Echo report.
7. Pulmonary, Mitral and Tricuspid insufficiency/regurg is present in basically everyone in trace amounts. The seals formed by the valves are never completely watertight. Given the dilation it is completely expected to find the regurg is a bit more than trace.
Generally regurg has 2 classifications, or types:
1. Secondary (Aka Physiologic or Functional) Regurg; this type of regurg occurs SECONDARY to some other condition such as Dilated CM, inflammatory disease, congenital condition or Myocardial Infarction.
Or it may occur in response to some other PHYSIOLOGIC condition or status.
The valve in this case is structurally normal and otherwise FUNCTIONAL.
2. Primary or Pathologic regurgitation. This occurs due to disease or malformation of the Valve itself. It is not opening or closing correctly, it has the inappropriate number or shape of leaflets or the leaflets are inappropriately fit together. Another possility in this category would be a failure or malformation of the mechanisms that hold the valve in place, e.g. chordae.
Severity, in terms of volume and hemodynamic consequence, of Regurg is always the number 1 consideration when assessing regurgitation and the possibility for any sort of itnervention on the valve directly.
The second consideration is the type of dysfunction. The focus of a secondary type of regurg would be on correcting the underlying issue, with correction of the valve only being necessary in cases in which the underlying disease cant be reversed or the regurg is severe to the point of hemodynamic compromise and development of symptoms or inevitable development of the same.
For actual primary valve diseases, the focus is on identifying the risk associated with each specific abnormality and outcomes of intervention.
Thankfully your case is simple! Secondary regurg with dilated CM.
8. As discussed the thinng relative to increased dilation does mot APPEAR normal. However, there are specialists that are significantly more knowledgable in this.
9. Enlarged livers from dilated hearts, dilated hearts from enlarged livers. Going back to the original point again, the right doctors devote a tremendous amount of effort to this study. I am not qualified to do much more then acknowledge your point that these things can be connected.
10. Chronic cough can be a symptom, yes. However 'Paroxysmal Nocturnal Dyspnea' and a decrease in exercise tolerance are the red flags. If you're still able to run 7 miles, any connection between the cough and the heart would be very premature and inappropriate.
As far as symptoms go; coughs are about as non specific as they get. Even when you KNOW you have an illness that causes coughs you can still discover you have something non related that caused it.
For example you can have known lung cancer... You get a cough. It would make sense that its related to the cancer right? Wrong! You go to the doctor and wind up diagnosed with Tuberculosis.. Because thats just the type of thing coughs are, unpredictable.
Despite the overwhelming temptation to do so, I wouldn't put much stock in Cough as far as evidence in favor of Dilated CM/ HFpEF goes.
11. Frequent urination is a sign of heart health for sure. When the muscles stretch they release chemicals called "natriuretic peptides". These chemicals are critical markers of the degree of dilation and are reguarly tested for in clinical laboratory.
The other symptoms, while nice to know, are also ambiguous. More specifc than cough, but not big indicators of your condition specifically.
Final Opinion\ Summary
I think you may benefit from a visit with a local cardiologist specializing in "Heart Failure" or "Structural Intervention". This can be accomplished by consulting either your general cardiologist or your pcm.
You should make every effort to get as much information, documentation, discs and images as you reasonably can and forward them to this specialist well in advance (2 weeks) of your appointment.
Anticipate repeat echos and labs. Medicine is unfortunately still a business after all.
In terms of your chief concerns I think they should be:
1. The dilation itsself
2. The increased urination
3. The liver enlargement
These 3 concerns best represent the likely underlying problem and support any future diagnosis the best.
I also think you should ask your doctor about getting put on a low dose beta blocker, i.e. Metoprolol 12.5 or 25, which will help ease your concerns regarding the couplets. Good luck!
1. I would agree it appears some degree of dilation is present. More important here would be resting blood pressure, symptoms, exercise capacity etc. All of which are normal for you. Your elevated decel time is important but your resting heart rate in addition to all the other diastolic factors, e/a, e/e' ivrt, a wave reversal, LA Volume etc. All need to be considered. When combined these factors will determine the best course of treatment (if any). In terms of what sort of treatment or action is required your general cardiologist or possibly a structural or heart failure specialist would best be able to determine that. As am EP person I would honestly feel a bit underqualified to give any opinion on that.
There is variability in operators results:
Interoperator variability between individuals of roughly equal experience is just shy of 10%.
With an experience gap 15- 20%
These figures have been studied and reproduced.
2. Pauses can suggest a problem yes. For you it is more likely autonomic given your athleticism. In this case it's sort of expected, which is encouraging. The real severity of the pause is indexed for heart rate. So in your case 5 seconds may not be as bad as 5 seconds in someone else. The decision to place a pacemaker is typically based off symptoms in this case. However the presence of such pauses could aid in a decision to pace the dilation down the line. Again its a multi disciplinary effort and I can really only speak for half of the equation.
In the absence of a cardiomyopathy there would be no justification to pace without symptoms. (Risk>benefit)
3. Normal finding. Trivial effusion is a common finding that doesn't even become an issue until it begins to have a hemodynamic effect. Some individuals experience this early, but most folks are able to compensate for fairly large volumes of Effusion. I really would just strike this one off the list as a concern.
4. Another one to cross off the list. 460 ms QTc, without symptoms or further prolongation on stress is absolutely positively not pathologic. That much I can vouch for confidently.
5. Everything you said about the couplet is true. Given the changes observed in the muscle of your heart we can even relatively certainly summise that this is the underlying cause.
How many couplets are concerning and what exactly we should do about them is a matter of debate. A single couplet is oninous but not imminently ominous, such as we would find in a patient with 3 or 4 couplets per hour.
Generally however the best course of action seems to be to identify the underlying cause of the couplets. If necessary from there we can try to target them with medical management. For a single couplet this strategy would be conservative. If unable to suppress, we can consider ablation and in extreme cases prophylactic ICD implant.
In your case I would agree with the assertion that ablation would absolutely be inappropriate. Aside from being invasive and hence carrying some risk, ablating the pathway will do no good without figuring out whats going on with the myocardium.
Basically ablating a circuit created by dilation without stopping the dilation will just create more scar tissue which is likely to just create anither circuit and hence another couplet. It doesn't really fix the actual problem or source of the phenomenon.
In terms of an ICD, again.. Multi disciplinary. On its own, not an indication.. Combined with a bunch of other things, maybe, pending the recommendation of the muscle guys.
Meds would be appropriate so long as there's no contraindications to do so.
There is variability in operators results:
Interoperator variability between individuals of roughly equal experience is just shy of 10%.
With an experience gap 15- 20%
These figures have been studied and reproduced.
2. Pauses can suggest a problem yes. For you it is more likely autonomic given your athleticism. In this case it's sort of expected, which is encouraging. The real severity of the pause is indexed for heart rate. So in your case 5 seconds may not be as bad as 5 seconds in someone else. The decision to place a pacemaker is typically based off symptoms in this case. However the presence of such pauses could aid in a decision to pace the dilation down the line. Again its a multi disciplinary effort and I can really only speak for half of the equation.
In the absence of a cardiomyopathy there would be no justification to pace without symptoms. (Risk>benefit)
3. Normal finding. Trivial effusion is a common finding that doesn't even become an issue until it begins to have a hemodynamic effect. Some individuals experience this early, but most folks are able to compensate for fairly large volumes of Effusion. I really would just strike this one off the list as a concern.
4. Another one to cross off the list. 460 ms QTc, without symptoms or further prolongation on stress is absolutely positively not pathologic. That much I can vouch for confidently.
5. Everything you said about the couplet is true. Given the changes observed in the muscle of your heart we can even relatively certainly summise that this is the underlying cause.
How many couplets are concerning and what exactly we should do about them is a matter of debate. A single couplet is oninous but not imminently ominous, such as we would find in a patient with 3 or 4 couplets per hour.
Generally however the best course of action seems to be to identify the underlying cause of the couplets. If necessary from there we can try to target them with medical management. For a single couplet this strategy would be conservative. If unable to suppress, we can consider ablation and in extreme cases prophylactic ICD implant.
In your case I would agree with the assertion that ablation would absolutely be inappropriate. Aside from being invasive and hence carrying some risk, ablating the pathway will do no good without figuring out whats going on with the myocardium.
Basically ablating a circuit created by dilation without stopping the dilation will just create more scar tissue which is likely to just create anither circuit and hence another couplet. It doesn't really fix the actual problem or source of the phenomenon.
In terms of an ICD, again.. Multi disciplinary. On its own, not an indication.. Combined with a bunch of other things, maybe, pending the recommendation of the muscle guys.
Meds would be appropriate so long as there's no contraindications to do so.
Concerns
1.) That the heart dilation and wall thinning is a precursor to dilated cardiomyopathy
Two hypotheticals concern me: First, that my heart muscle is/was weakening and this remodeling is a response to such that is temporarily delaying an inevitable loss of function. Second, that my heart is actually fine, but some other problem of a non-cardiac origin is causing a fluid overload in my body which is forcing my heart to stretch out, and that eventually this will put so much strain on an ever stretching/thinning heart that it will begin to weaken and become dysfunctional. (see “key abnormalities on cardiac MRI for further details)
2.) That my sinus pauses are indicative of an electrical/conduction abnormality that will result in a nocturnal cardiac arrest (see “key abnormalities on Holter strips” section for further details)
3.) That my palpitations are indicative of electrical instability that may predispose me to reentrant arrhythmias that would degenerate into a full cardiac arrest (see “key abnormalities on Holter strips” section for further details)
4.) That the pericardial and pleural effusions are indicative of the beginnings of heart failure
5.) That the valve regurgitation is a sign of deteriorating heart function
6.) That my QT interval suggests I’m prone to afterdepolarization-induced, potentially lethal arrhythmias.
1.) That the heart dilation and wall thinning is a precursor to dilated cardiomyopathy
Two hypotheticals concern me: First, that my heart muscle is/was weakening and this remodeling is a response to such that is temporarily delaying an inevitable loss of function. Second, that my heart is actually fine, but some other problem of a non-cardiac origin is causing a fluid overload in my body which is forcing my heart to stretch out, and that eventually this will put so much strain on an ever stretching/thinning heart that it will begin to weaken and become dysfunctional. (see “key abnormalities on cardiac MRI for further details)
2.) That my sinus pauses are indicative of an electrical/conduction abnormality that will result in a nocturnal cardiac arrest (see “key abnormalities on Holter strips” section for further details)
3.) That my palpitations are indicative of electrical instability that may predispose me to reentrant arrhythmias that would degenerate into a full cardiac arrest (see “key abnormalities on Holter strips” section for further details)
4.) That the pericardial and pleural effusions are indicative of the beginnings of heart failure
5.) That the valve regurgitation is a sign of deteriorating heart function
6.) That my QT interval suggests I’m prone to afterdepolarization-induced, potentially lethal arrhythmias.
KEY ABNORMALITIES ON CARDIAC MRI
LVEDV: 200mL (117mL previous, 154mL normal cut-off): This is the amount of blood in my left ventricle just before the start of each heartbeat. The left ventricle pumps blood out to the body
LV Mass: 114g (181g previous): This is the weight of my left ventricle. It has shrunk a lot.
LVEDD: 6.0cm (4.6cm previous, 5.4cm normal cut-off): This is the width of my left ventricle. It has dilated a lot.
IVS and LV wall thickness: 0.5/0.5cm (1.1/1.1cm previous, 0.6cm low normal cut-off): This is the thickness of the left ventricular wall and the wall separating the left and right ventricle. They’ve become much thinner.
SV: 123mL (61mL previous, 100mL normal cut-off): This is how much blood I pump out with each beat. It’s become high enough that it’s putting abnormal stress on the heart.
LA Volume: 134mL (51mL previous, 58mL normal cut-off): This is the amount of blood in the left atrium before it begins filling into the left ventricle. The left atrium receives blood from the lungs and sends it down to the LV to be pumped out to the body.
RA Volume: 144.5mL (no prior reference, normal cut-off 40mL): This is the amount of blood in the right atrium. It receives deoxygenated blood that returns to the heart after circulating the body and having its oxygen used along the way; the RA sends it to the right ventricle, which pumps it back to the lungs to be reloaded with new oxygen.
RVEDV: 236mL (no prior reference, 160mL normal cut-off): This is the amount of blood in the right ventricle before it pumps back to the lungs.
RVEDD: Measurements not provided, but impression said to be dilated: This is the width of the right ventricle.
CARDIOLOGIST'S FINDINGS/NOTES/IMPRESSIONS FROM MRI
RV Size: Dilated
RV Function: Normal right ventricular systolic function. There are no regional wall motion abnormalities. Specifically, no aneurysmal or dyskinetic segments are noted.
RV Hypertrophy: None
RV Other: No mass or thrombus is noted
-------------------------------------------------------------
LV Size: Moderately dilated
LV Hypertrophy: None
LV global function: Normal left ventricular systolic function. There are no regional wall motion abnormalities
LV Other: No mass or thrombus is noted
----------------------------------------------------------------
Left Atrium: Dilated
Right Atrium: Dilated
--------------------------------------------------------------
Valves: There is tricuspid and pulmonic regurgitation present (severity not assessed)
Aorta: The aortic root, ascending aorta, and descending aorta are normal in size
Pericardium: Trivial pericardial effusion
Other: Small bilateral pleural effusions noted. Normal pulmonary venous anatomy with four pulmonary veins seen draining into the left atrium.
Rest Perfusion: Normal
Late gadolinium enhancement: There is no significant delayed enhancement to suggest LV or RV scar, fibrosis, or prior infarct
Summary:
1.) The right ventricle is dilated (RVEDVI=129.3mL/m2) with normal systolic function. RVEF=55.8%. There are no regional wall motion abnormalities. Based on the modified Task Force Criteria there is no MRI evidence of ARVC/D
2.) The left ventricle is dilated with normal systolic function=61.7%
3.) Bi-atrial enlargement
4.) Normal rest perfusion
5.) No evidence of LV or RV scar or fibrosis
6.) Small bilateral pleural effusions
LVEDV: 200mL (117mL previous, 154mL normal cut-off): This is the amount of blood in my left ventricle just before the start of each heartbeat. The left ventricle pumps blood out to the body
LV Mass: 114g (181g previous): This is the weight of my left ventricle. It has shrunk a lot.
LVEDD: 6.0cm (4.6cm previous, 5.4cm normal cut-off): This is the width of my left ventricle. It has dilated a lot.
IVS and LV wall thickness: 0.5/0.5cm (1.1/1.1cm previous, 0.6cm low normal cut-off): This is the thickness of the left ventricular wall and the wall separating the left and right ventricle. They’ve become much thinner.
SV: 123mL (61mL previous, 100mL normal cut-off): This is how much blood I pump out with each beat. It’s become high enough that it’s putting abnormal stress on the heart.
LA Volume: 134mL (51mL previous, 58mL normal cut-off): This is the amount of blood in the left atrium before it begins filling into the left ventricle. The left atrium receives blood from the lungs and sends it down to the LV to be pumped out to the body.
RA Volume: 144.5mL (no prior reference, normal cut-off 40mL): This is the amount of blood in the right atrium. It receives deoxygenated blood that returns to the heart after circulating the body and having its oxygen used along the way; the RA sends it to the right ventricle, which pumps it back to the lungs to be reloaded with new oxygen.
RVEDV: 236mL (no prior reference, 160mL normal cut-off): This is the amount of blood in the right ventricle before it pumps back to the lungs.
RVEDD: Measurements not provided, but impression said to be dilated: This is the width of the right ventricle.
CARDIOLOGIST'S FINDINGS/NOTES/IMPRESSIONS FROM MRI
RV Size: Dilated
RV Function: Normal right ventricular systolic function. There are no regional wall motion abnormalities. Specifically, no aneurysmal or dyskinetic segments are noted.
RV Hypertrophy: None
RV Other: No mass or thrombus is noted
-------------------------------------------------------------
LV Size: Moderately dilated
LV Hypertrophy: None
LV global function: Normal left ventricular systolic function. There are no regional wall motion abnormalities
LV Other: No mass or thrombus is noted
----------------------------------------------------------------
Left Atrium: Dilated
Right Atrium: Dilated
--------------------------------------------------------------
Valves: There is tricuspid and pulmonic regurgitation present (severity not assessed)
Aorta: The aortic root, ascending aorta, and descending aorta are normal in size
Pericardium: Trivial pericardial effusion
Other: Small bilateral pleural effusions noted. Normal pulmonary venous anatomy with four pulmonary veins seen draining into the left atrium.
Rest Perfusion: Normal
Late gadolinium enhancement: There is no significant delayed enhancement to suggest LV or RV scar, fibrosis, or prior infarct
Summary:
1.) The right ventricle is dilated (RVEDVI=129.3mL/m2) with normal systolic function. RVEF=55.8%. There are no regional wall motion abnormalities. Based on the modified Task Force Criteria there is no MRI evidence of ARVC/D
2.) The left ventricle is dilated with normal systolic function=61.7%
3.) Bi-atrial enlargement
4.) Normal rest perfusion
5.) No evidence of LV or RV scar or fibrosis
6.) Small bilateral pleural effusions
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