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Please do not hesitate to contact Dr. Matthews regarding any heart problems or symptoms, which you desire to discuss. He will gladly answer as promptly as possible!
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On this page we include some discussion threads with Dr. Matthews that may have broad appeal.
Specific names have been omitted to preserve the anonymity of the writers.

E-mail received:

My dear friend is a 94 y.o. cauc female with a history of myocardial infarction at 39, with angina pectoris since then, infrequently, hypertension, and three months of atrial fibrillation. She is on 7.5 mg. of coumadin QD with an INR of 2.2. Six hours post cardio-conversion she was experiencing nausea, some retching, no vomiting, when her L. iris turned purple! She first noticed a decrease of vision in that eye, evidenced by shutting one eye, then the other. This was a sudden onset. After about 30 minutes, she could see through the purple, though she said everything looked as if she were looking through a purple curtain. Within another 30 minutes, her O.D. had purple vision without the coloration. An ultrasound was negative for clot. Is this a common phenomenon? The physicians in the hospital will not address that question! Her vision is still not returned to WNL though she has been released. Your replies will, obviously, not be considered final or definitive, but any further information will be greatly appreciated. Sincerely,

Dr Matthews response:

Was she on any other medication! The sudden loss of some of the vision in left eye, the change in the appearance of the eye(?was this "blood" like a hemorhage), and the seeing of a purple color in her vision (was she seeing blood or was the purple actually involving objects away from her)are worrisome. Was an opthalmologist called to see her!It sounds like she threw a small embolus from the heart to the eye or occipital area of the brain, for which occurrence the coumadin was being given to prevent. Or perhaps, there was increased pressure in the eye from the retching, causing her to bleed into the eye! Was an MRI of the eye and brain done! Was she seen by a neurologist? Did they increase her coumadin dose? How common? I don't know, but it is unusual.RJM

E-mail received:

I am doing a science project on music and its effects on heartrate. I would like to know if there are any studies on this topic and if so, what do they show? Thank you.

Dr Matthews response:

I can recommend consulting medical school libraries for the data you seek. Depending on the effects of the music on the sympathetic and parasympathetic nervous systems as to whether it calms or excites the subject, one might expect changes in the heart rate, as more or less epinephrine, norepinephrine, cortisone etc are released.This response would be based on what the music meant to the individual, which may be variable from one to the next, due to past experiences.RJM

E-mail received:

Dear Sir, I experienced rapid pounding of the heart for a few seconds in the past few weeks. I went to a cardiologist and he has taken ECG and EchoCardiogram. Everything appeared to be normal, but even today, i faced a problem wherein, the rapid pounding of heart started immediately after i woke up. This sort of rapid heart beat comes to me only after i wake up from sleep in the morning. The doctor has prescribed ciplar 10mg (1,1 morn, evening) for a month. Please do indicate what more steps i need to take in wake of this.... can i have permanent relief soon? awaiting your earliest reply, regards

Dr Matthews response:

Also, how old are you? Are there any associated symptoms?What happens when you run?What is your cholesterol? Do you smoke cigarettes, grass, drink coffee, alcohol, soft drinks with caffeine? What is your heredity? Have you had a 24 hour ECG Holter recording and a stress treadmill ECg test? Please read on my site under messages the subject of palpitations: I think you may be having "premature atrial contractions", which are causing you to have palpitations(defined below). WHAT ARE PALPITATIONS? Palpitations is a disagreeable awareness of the heart beat, often described as a pounding, stopping, jumping, or racing in the chest. The sensitivity of the nervous system determines whether or not the patient complains of palpitations, which are not related to the seriousness of the heart disease or the type of arrhythmia. When patients have a premature heart contraction(PACs), they feel the post-extrasystolic beat, associated with a large stroke volume, which is due to the longer filling period in diastole. A patient may be aware of a cardiac arrhythmia by detecting an uncomfortable sensation in the neck. They may complain when the heart beat is slow or fast, and when it regular or irregular. Annoying palpitations are common symptoms of premature atrial contractions(PACs) in patients who have either no underlying heart disease or mitral valve prolapse. Reassuring the patient of the benign nature of the arrhythmia may suffice, and no therapy is necessary other than removal of the inciting factors such as cigarettes, coffee, alcohol, and excessive fatigue. When palpitations are sufficiently annoying that an intervention must be considered,a low dose of a beta-adrenergic blocking agent is preferred to more aggreessive (more dangerous) membrane-active antiarrhythmic agents. When it is necessary to treat PACs to prevent initiation of sustained arrhythmias or because of intolerable palpitations, convential antiarrhythmic agents may be effective. Depending upon tolerance and side effects, any of the membrane-active drugs or beta-adrenergic blocking agents may be considered. Also, Please go to my site at http://www.rjmatthewsmd.com/Definitions/PVCs.htm Dr.Matthews

E-mail received:

I am 27 years old symptoms-rapid pounding of heart only when changing from sleep mode to wake mode...nowhere else do i get the palpitations...random slight chest pain...mostly in the right chest..i cant sleep on my stomach putting pressure on my heart, it pains sometimes...so i sleep on my right side.. nothing happens while running...no palpitations have not measured cholestrol levels i do not smoke or drink...but drink 4 cups of coffee a day... my mother has high blood pressure...grandmother...high bp and diabetes...i dont think anybody had heart disease is a stress ecg and holter monitor required for my condition? sir, one more thing to add, even yesterday night, i felt palpitations when i woke up after sleep, but they quickly stopped probably bcoz of effect of tablet...sir, till what time should i continue taking proparanol tablets? is this a permanent cure? or i need to continue taking them? also my job is working long hours..do you have any advise on how to go about things? regards

Dr Matthews response:

Inderal is a good drug! If you stop the coffee, you may be able to stop the inderal, But of course consult your cardiologist. Certainly the tests can be done if your symptoms persist! Did you read the data I sent to you and consult my web site?RJM

E-mail received:

Sir, sorry for the delay in writing back..was in transit...i had read the data u sent and subsequently went thro' ur website....was really very informative...thankx for the wonderful guidance you have given to me... looking forward to keepin in touch with u doctor... regards

E-mail received:

First, I recently had a cardiac MRI. The conclusions were: 1. Moderate left ventricular global dysfunction with an ejection fraction of 44% 2. Dipyridamole RMI perfusion stress test showing evidence of inferolateral ischemia. 3. No evidence of cardiac sarcoid. I had this test performed at a hospital in NJ and I can't get in touch with the cardiologist -- the practice is too big and no one is returning phone calls. Should the above results cause me concern? Also, if treatment is necessary, what should I be looking for from my doctor? Can you define (if you have time) what the above conclusions (#1 and #2) mean? Thanks!

Dr Matthews response:

It does should serious! The dysfunction and the reduced ejection fraction indicate htat your left ventricle is wekened and not pumping blod out of your heart as it should. The normal Lv ejection fraction should be 50% or greater! Apparently your left ventricle is not relaxing properly. The inferolateral ischemia means that you have coronary artery disease due to atherosclerosis to an extent that you are nt getting enough blood to the heart muscle in that area, possibly supplied by the circumflex artery or the ribght coronary artery. You need your cholesterol checked .And you need to undergo the standard nuclear stress test with the treadmill to confirm what they say you have! You also need an echocardiogram! If the results are confirmed ,you will need a coronary angiogram to locate the the blockage, which can be treated with a balloon angioplasty and stent or bypass surgery!rjm

E-mail received:

Hello! I am a psychiatrist in C-L psychiatry. I would like to know what you think about depression as a precursor of myocardial infarction. Thanks

Dr Matthews response:

I am not knowlegible enough to know what C-L psychiatry means as compared to just psychiatry! Nevertheless, a quick review reveals in one study that coronary artery disease (CAD) was more prevalent among mental patients diagnosed as suffering from depression than among other patients. Anxiety and depression or other psychological changes can precede or follow cardiac disasters. Persons having higher scores for depression on psychological tests may be more likely to have a myocardial infarction than those scoring below the mean, and sudden death in women may be more common in those who have had a mental illness. Sleep disturbances, often a sign of depression, have been reported to be predictive of future angina and infarction. In a large follow-up of patients diagnosed with neurosis the relative risk of death was higher than expected for all causes (but mainly suicide and accidental death). Among diseases related to the arteriosclerotic process, the relative risk was 1.6. The greater use of cigarettes was considered to be a factor in these deaths as well as in the increased mortality from respiratory system diseases. Plasma cortisol levels tend to be parallel depressive moods eveni n normal persons and may be significantly elevated in persons diagnosed as depressed.RJM

E-mail received:

I am a student studying physiology and I have a couple questions that I wanted to ask regarding heart rate and blood pressure:1) Why is the heart rate and blood pressure decreased in a person who is lying down in the supine position? What happens to the heart rate and blood pressure when that person stands up after lying down? 2) Why does heart rate and blood pressure go up with exercise? What would the differences be in the EKG with exercise? 3) If one placed their hand in ice cold water, affecting pain fibers, why would this cause a decrease in heart rate and an increase in blood pressure? What is the mechanism behind this response? How can we acquire further evidence for this mechanism? 4) What is an atrial natriuretic factor? What is its significance? Thank you!

Dr Matthews response:

Many factors contribute to variations in an individual's blood pressure during daily activities.These include (1) body posture; (2) state of muscular, cerebral, or gastrointestinal activity; (3) emotional or painful stimuli; (4) environmental factors such as temperature and noise level; (5) the use of tobacco, coffee, and other drugs with direct or neurally vasomotor properties. The average diurnal pattern of blood pressure consists of an increase throughout the day and early evening and a significant, rapid decline to a low point during the early,deep stage of sleep. With normal respiration the peak systolic blood pressure is greater during expiration by as much as 10mmm Hg than during inspiration. Isotonic exercise in both the supine and upright position produces a moderate increase in blood pressure. Sustained isometric muscular contraction produces an abrupt increase in blood pressure. The fourth major determinant of cardiac function is the heart rate,which is the major mechanism by which most people increase their cardiac output during periods of modest increased demand or exercise. An increase in heart rate may also increase myocardial contractility and relaxation and improve diastolic performance. Presumably, the increase in heart rate results in the release of more Ca++ from stores within the myocardial cell to enhance myofibrillar contraction. Sitting ,standing,or strain of the Valslva maneuver decreases left ventricular volume( while venous return decreases) and as a compensatory action to keep the cardiac output constant, the pulse rate and/or the blood pressure may rise. Maneuvers such as squatting, vasopressure infusion,and the supine position increase left ventricular volume,as the venous return and afterload increases, and the pulse rate may decrease as a result. In the cold pressor test,intense discomfort is produced by the immersion of the hand in ice water. Reflex sympathetic stimulation is produced, resulting in a rise in systolic blood pressure accompanied by a modest rise in heart rate. This elevation of the rate-pressure product increases cardiac work,i.e., Myocardial O2 demand,which is met by an increase in coronary blood flow.But in patients with coronary disease,there is a paradoxical decrease in coronary blood flow. The discrepancy between myocardial O2 demand and supply is the basis for angina in this case. You can consult the medical school library for further information on this mechanism, as well as the atrial naturetic factor (especially the recent literature). With work there is a need for increased cardiac output to supply enough O2 to the myocardium, which is accomplished by the pulse and the BP going up.The ECG in such circumstances shows the pulse rate increasing as expected.RJM

The atria produce atrial natriuretic peptides (ANPs) that have natriuretic and diuretic actions and relax intestinal muscle.Some of them also relax vascular muscle.It is probable that atrial distention triggers the release of ANP, leading to diuresis and natiuresis.ANPs also inhibit the production of aldosterone. The concentration of ANP is increased in heart failure. This should produce a natriuresis by its direct renal action(particularly since it decreases aldosterone production).However,it appears that the homeostatic control of circulatory blood volume is inadequate to overcome the stronger forces tending to retain sodium and water in heart failure. ANP also inhibits renin and arpinine vasopressin (AVP).Many with heart failure do have increased plasma concentration of ANP, presumably released secondary to atrial distention, but their natruretic and vasodilator properties are overwehlmed by stronger factors producing retention of salt and water and vasoconstriction. ANPs are made and stored in specialized atrial cells(some may come from ventricular myocytes), from which they are released by the stimulus of atrial distention. Some have both a natriuretic and a diuretic effect, and some relax vascular smooth muscle. They may be released in response to extracellular fluid expansion and hence are increased in dialysis patients.

E-mail received:

Dear Dr I was diagnosed to have a problem known as PVCs of unknown eteology. I used to get 10 - 15 PVCs per minute. After that I was put on Metoprolol and the frequency came down to 1 or 2 per minute. Now I get PVCs when I swallow / drink something. PVCs frequency goes up when I consume beer / alcohol / tea coffee more than normal. My BP was 160 / 100 when I started the drug ( Sept 1999) which has now stablised around 140 /90 Pl advise if I can continue with Metoprolol 50 mg one a day.Thanks

Dr Matthews response:

Do not stop the medication unless advised by your own physician, it should be safe to stop the alcohol, tea, coffee, beer.RJM

E-mail received:

Dr. Matthews, Nice site, thanks for providing the service. I have a few questions. I am 23 year old female and have been experiencing near black outs for as long as I can remember. Usually occur when I am standing, start seeing twinkling lights and ringing in my ears. I can usually get it to stop if I squat down for about 5 minutes. Sometimes that doesn't work. I always feel a tad nauseous and very tired after one happens. I am currently doing the 1 month monitoring thing to try and catch an episode. I think I caught on the other day and sent it in. The techseemed concerned but did not say why. She told me my heartrate was 160, at the time I was running levels, acting as the rod person. Have to hold the rod level so the person reading it can get the number as accurate as possible. Have to stand very still. I think I started walking back to my partner when it was still recording. I was not really walking that fast cause I strained my knee a week ago. I swim regularly and I don't understand why, just standing or walking would make it go up so high. I did experience a touch of dizziness but nothing like I have experienced in the past. Would casual walking make a normal heartrate go that high? I have a 5k open water swim in another week, is it okay to do it? I have always gotten really red and very dizzy after exercising but it doesn't stop me from participating in a sport I love. I have asked my cardiologist all of these questions and he said all of this could be from two things. Never said what those two things were though. I am suppose to go back soon but I guess I just want reassurance that it's okay to swim this race and to find out if 160 is a normal rate for standing or casual walking. I would really appreciate your opinion. Thanks so much! Sincerely,

Dr Matthews response:

It shoulds like you have postural hypotension due to standing too still during your work of running rod tests (what is a rod test?), in which you say that you have to stand very still for the the assistant to read the numbers. I believe you are getting too much venous pooling of blood in your lower extremities, which results in reduced return of blood to your heart and hence a decreased output of blood to your brain,and hence the symptoms. It is important to avoid dehydration and any drug (medication) which may reduce blood volume like diuretics, for example. You must arise slowly from a recumbent or sitting position. It is important to flex the calf muscles when assuming the upright position. You must avoid prolonged immobility during standing (so what you are doing with the rod test may be inducing the symptoms. Use of elastic hose foot to groin may be helpful. Also, increasing the salt in you diet may expand the blood volume and help prevent the symptoms (or the use of Flourocortisne). Squatting increase the venous return to the heart (similar texercising the calf muscles to increase venous return to the heart), which becomes larger and the afterload on the heart increases. In view of the above discussion, swimming,which is a recumbent exercise,should be good for you, as it should increase the venous return to the heart.I can not confirm the rapid rate unless your physician verifies it.It may be that your standing so still with the venous return dropping caused your heart to pump faster to compensate! Finally, the above is not a diagnosis, since I have not examined you or your test results.So you must talk to your cardiologist to get the real professional advice on your condition.Dr.Matthews

E-mail received:

Dear Dr. Matthews, My job involves surveying the land. Being the "rod man" means holding a graduated surveying rod as level as possible. Readings are into the thousandths ( 4.568). Holding the rod that still only involves standing still for a few seconds. When we are in the field I take a gallon of water with me and I am always drinking. I live in Florida and was a lifeguard so I really know about dehydration. I also shift my weight around when acting as rod man or even just standing around talking to family, that still doesn't do much to prevent it. Even walking doesn't seem to abate it right away. Is 160 a normal rate for a 23 year old woman when she is standing? Also is 120 a normal rate for one laying on a couch relaxing? I appreciate your candor and knowledge, thank you. Sincerely,

Dr Matthews response:

No, those rates are not normal,but need to be documented as the Holter has or event recorder will! Also, the stress echocardiogram or stress thallium nuclear test may be in order, as well as the tilt test. Never the less ,postural hypotension seems like a good answer, unless a cardiac arrhythmia is found! You should have thyroid tests, blood sugar, electrolytes, bun,liver function tests calcium, phosphorus, cbc, urinalysis.and lipids checked! Reread the first e-mail re treatment of postural hypotension! Dr.Matthews

E-mail received:

Dear Sir, I have a dilated cardiomyopathy and I've read in the newspapers that it can be treated by muscle cells implantation in cardiac muscle via transcatheter. If this is right, do you do this kind of operation in your center ? and if you do it, what I have to do to make it ? Waiting for your reply, Thanks in davance and best regards,

Dr Matthews response:

I have not heard of this research. But if you can tell me where it is being performed according to your newspaper I will investigate!Dr.Matthews

E-mail received:

Dear Dr.Matthews, Thank you very much for your reply, I really do appreciate it. I've read it on May in an arabic newspaper, it states that they succeed in France to treat heart failure through cell implantation in cardiac muscle (they didn't mention through Transcatheter but I knew it from my doctor). I don't know where this medical center is exactly located in France but I know that they 've made a progress in this field. I tried to search on the net for similar sites to reach a place in which I can have this treatment as my physician told it's the only hope for me (either to make limitated effort using medication or to do this implantation, my heart muscle effiency is less than 25%). I found a company in the States called BIOHEART, I'm sure you know it. They have clinical programs in Netherlands and Germany. I 've sent them 2 emails but they don't answer. I was willing to go to Germany as I live in Warsaw to make this trial but I receive no reply though I meet the conditions [The conditions stated in the clincal programs : dilated cardiomyopathy, in stable conditon under rest , age 61, class III , available to follow up visits and willing to sign a consent " if there is no danger"]. That is the case, so I don't know what I need to do? Waiting for your instruction, With my best regards,

Dr Matthews response:

Please send Bioheart's e-mail address and I will try to contact them!RJM

Dr Matthews response:

Dr.Haimes, A desperate man with dilated cardiomyopathy e-mailed me regarding how he could contact Bioheart,Inc. to investigate the possiblity of being a patient in the company's treatment experiments using the muscle implants in certain patients with heart disease. I would appreciate you contacting this patient.... to explain how he might contact the medical doctors carrying these treatments. I am a cardiologist in Los Angeles,Ca. Thank you,Robert J. Matthews,MD

E-mail received:

What does it mean when a doctor says she hears a split s2 beat?

Dr Matthews response:

Normally during expiration, A2 (aortic valve component of second sound) and P2(pulmonary valve component of second heart sound) are separated by an interval of less than 30ms and are heard by the doctor as a "single" sound. During inspiration, both components become distinctly audible as the splitting interval widens, primarily due to a delayed P2.The delayed P2 and the early A2 are due to a complex interplay between dynamic changes in pulmonary vascular impedance and changes in systemic and pulmonary venous return. The net effect of these changes is the prolongation of the right ventricular ejection and a concomitant decrease in left ventricular ejection that results in widening of the splitting interval during inspiration. The splitting of S2 is usually best heard at the second or the left intercostal space. Abnormal splitting of S2 exists when there is the audible expiratory splitting (more than 30ms), that is the ability to hear two distinct sounds during expiration .Dr.Matthews

E-mail received:

What tests or procedures would you perform in the following patient: 61 yr. old with 15 year old porcine aortic valve done in 1979.(asymptomatic until 11th yr. - angina). Patient had echo & treadmill exercise test with thaillum injection. Report revealed EST of 11/2 ST depression, impaired diastolic function and concentric LV hypertrophy. On 01/93, patient had mild shortness of breath. On 12/93, patient had much more shortness of breath, coughing, difficulty breathing lying down. Echo was done (moderate left atrial enlargement, trivial MR, aortic valve functioning well.) Medication changed from Tenormin to Capoten. Patient was not better after six months. Echo repeated reading: severe diffuse myopathy of LV with chamber enlargement, AVA of 1.2 cm, gradient of 20 and moderate to severe MR. Any input would be helpful. Thank you.

Dr Matthews response:

A stress thallium test with adenosine or exercise to restudy for coronary atherosclerosis progression, since prior test showed ischemia(ST depression on the ECG) apparently due to coronary atherosclerosis? There is no mention of what defects were seen on the thallium pictures (if any)! If still positive for ischemia,consideration of coronary angiogram to confirm and locate the obstruction in the particular coronary artery would be a possible next step,hopefully prior to onset of symptoms of congestive heart failure. If there was a significant obstruction,one might request a surgical opinion regarding a bypass (hopefully prior to the the development of congestive heart failure), or better yet consider angioplasty with stent insertion into the involved artery first. Since I do not have all of the data (nor its complete chronologic progression) and have not seen and examined the patient, the preceding thoughts are purely speculative and not of much clinical value. Was the mitral regurgitation and LV enlargement due to a prior myocardial infarction and diffuse coronary disease,injurying among other parts the posterior papillary muscle to the mitral valve?RJM

E-mail received:

I work as a transcriptionist. Is there such a thing as in-stant restenosis? What is it? I assume from dictation it is stenosing of a vessel after a stent has been previously placed. Thank you for help in this regard.

Dr Matthews response:

Perhaps it means that the stent had already stenosed one time, had repeat angioplasty for the stenosis, but the stent restenosed a second time after the relief of the angioplasty, like with Dick Cheney?RJM

E-mail received:

What tests or procedures would you perform in the following patient: 61 yr. old with 15 year old porcine aortic valve done in 1979. (asymptomatic until 11th yr. - angina). Patient had echo & treadmill exercise test with thaillum injection. Report revealed EST of 11/2 ST depression, impaired diastolic function and concentric LV hypertrophy. On 01/93, patient had mild shortness of breath. On 12/93, patient had much more shortness of breath, coughing, difficulty breathing lying down. Echo was done (moderate left atrial enlargement, trivial MR, aortic valvefunctioning well.) Medication changed from Tenormin to Capoten. Patient was not better after six months. Echo repeated reading: severe diffuse myopathy of LV with chamber enlargement, AVA of 1.2 cm, gradient of 20 and moderate to severe MR. Any input would be helpful. Thank you.

Dr Matthews response:

A stress thallium test with adenosine or exercise to restudy for coronary atherosclerosis progression, since prior test showed ischemia (ST depression on the ECG) apparently due to coronary atherosclerosis? There is no mention of what defects were seen on the thallium pictures(if any)!If still positive for ischemia,consideration of coronary angiogram to confirm and locate the obstruction in the particular coronary artery would be a possible next step, hopefully prior to onset of symptoms of congestive heart failure.If there was a significant obstruction,one might request a surgical opinion regarding a bypass (hopefully prior to the the development of congestive heart failure), or better yet consider angioplasty with stent insertion into the involved artery first. Since I do not have all of the data (nor its complete chronologic progression) and have not seen and examined the patient, the preceding thoughts are purely speculative and not of much clinical value. Was the mitral regurgitation and LV enlargement due to a prior myocardial infarction and diffuse coronary disease,injurying among other parts the posterior papillary muscle to the mitral valve?RJM

E-mail received:

Hi IM a student at Norte vista high school I would like to be a heart surgeon one day. I would appreciate your help with the questions IM about to ask.. What is the history of cardiology? What are the typical duties for a person with this career? Are you going to specialize? what are the requirements of this position, including physical and mental? What is the work schedule for this type of career? Is there an opportunity for advancement in this career? What is the salary rang and the benefits that are associated with this career? what kind of education do you need to have in order to have this career? what high school or college/university courses are necessary? what types of degrees are offered for this career? how many years of education? what is the cost of the education? what colleges / universities offer the necessary courses? what type of training is required for this type of career? how much does it cost? where can you achieve this training? is an internship required? what are the usual methods of entering this profession? is their a demand for new people in this field? what opportunities for experience exist for career exploration? what opportunities for advancement are there in this career? how does this career relate to chemistry? what part of chemistry will you be practicing? What does this line of work have to do with chemistry? What skills did you have in high school that were helpful in this career? What type of lifestyle does being a heart surgeon give you?
Please help me. I'm really interested in this field maybe one of your qualified and respected surgeons can help me. Thank you so much you can't imagine how much this E-mail coming from you will help me please SOS ASAP E-MAIL ME BACK!

Dr Matthews response:

I am not a heart surgeon, but a cardiologist, who deals with the medical management of heart problems including invasive, interventalistic procedures (stents, for example). But as a student you must first get throuh highschool with an exceptional grade point average to enter a university for premedical courses. The competition is fierce to enter medical school to become a physician, so you must be an excellent student with a very high grade point average. In medical school the competition continues. Most make it through medical school to become physicians. But after an intership, you have to decide how you want to specialize, surgery or medicine. These sort-after positions are hotly contested and in short supply! The rewards are also dependent not only on your individual, professional effort, but also where you live in terms of economics, competition and your ability to manage your financial affairs.Dr.Matthews

E-mail received:

Dear Dr: During a recent stress test my mother-in-law's Doctor told her there was evidence of ischemia. He subsequently scheduled an angioplasty and insertion of a stent for a vessel which we knew was 75% blocked. (She had another vessel stented in eary September) What does the "evidence of ischemia" mean? Thank you.

Dr Matthews response:

Depending on how the stress test was done, it means that the ECG showed ST changes, the echo.wall motion abnormalities, and/or the nuclear test transient filling defects on the films during exercise!Dr.Matthews

E-mail received:

Could you explain in layman terms just what st elevation is and what to do about it.i recently went thru surgury on sept 18 2001. and since then went to a rehabilitation center to return to work. had to wear a heart monitor for 24 hrs during sleep and strenous workouts at the center.and the cardiologist read the monitor and send back info saying that the st elevations were high.i had 3 stents put in and had one blockage angioplasty.so please could you give me all the information you have on this question.im a male 43 yrs old if that means anything.

Dr Matthews response:

If you click on definition "electrocardion (ECG) and resting ECG" on my website, you can find a complete discussion of ST elevation.The ST segment of the ECG comes after the QRS wave of the ECG has been inscribed. Normally the ST segment is at baseline on the ECG (isoelectric). If it is above baseline, then it is abnormal and can represent a current of injury to the heart muscle. So presumably the ST elevation on your ECG represent a recent injury to your heart muscle due to a recent heart attack(myocardial infarction), probably before you had your stents placed. It will take time for them to disappear. If it persist for a long time, it may mean that the heart attack caused a thinning out of the heart muscle, which then dilated in a localized area to be called an aneurysm.rjm

E-mail received:

dr matthews thank you for your reply back. but i went back to the page with definitions on it and cant find electrocardion.(ecg)and resting ecg on the website. could you give me the exact website your talking about. the correct address to bring it up.

Dr Matthews response:

It is www.rjmatthewsmd.com.You should be able to find the data!rjm

E-mail received:

I have been diagnoised with afixed anterosepatal defectwill it require surgery?

Dr Matthews response:

Perhaps, there is a buildup of cholesterol fat and calcium in the left coronary artery opening, which is beginning to block the flow of blood to the anteroseptal wall of your heart. The best thing to do is talk with your doctor and learn from him what is the problem in more detail! Dr.Matthews

E-mail received:

the doctor told me it was somehting growing from the wall of my heart and he thinks it might be starting to shut off the flow of the blood.what is a congenital defect this problem was not there 3 yrs ago when i had a stress test done please help me to understand this problem .

Dr Matthews response:

I suspect the defect is due to a prior myocrdial infarction.I assume the doctors will want to do an angiogram to see which artey is blocked and then decide on the best treatment for you either by- pass surgery or to do angioplasty and insert a stent. Have you had chest pain high cholesterol, strong family history of heart attacks or what? DR.Matthews

E-mail received:

Hi. I am a senior in high school this year. In order to graduate we are required to do a senior project. I decided to do mine on cardiology to benefit me in the future. I want to be a cardiologist when i grow up. I was hoping if I can send you a interview about your occupation. It would mean a grat deal to me. Thank You for your time. Sincerly,

Here are some questions I put together:1) How did you become interested in this field? 2) What type of education does one need to be a cardiologist? 3) Are there any additional requirments other than education for this career? 4) What is the availability of jobs for a cardiologist? 5) What are some advantages of being a cardiologist? 6) Are there any disadvantages? Explain. 7) What is the salary range? 8) What are the working hours? 9) What additional oppurnities are available? 10) What are the benefits of this career; for example: vacation time, sick leave, retirement plan, overtime, and workman's compensation? Thank You for helping me!

Dr Matthews response:

1. My teachers in highschool encouraged me to enter a profession, and I chose to become a physician. Ultimately, in medical school I favored internal medicine. Then in my internship I liked the challenges posed by heart patients in terms of diagnosis and treatment. So I decided to pursue cardiology. 2. After highschool, and having passed the entrance college examination, I consulted a premedical adviser, who mapped out the courses in zoology, anatomy, physics, chemistry, mathematics, and liberal art sciences, and foreign languages, which I would need to qualify to be a candidate to apply to medical school. Of course, one has to pass the medical school curriculum to become a physician and then to be successful in getting a position in a training hospital successively as an intern for a year, one to two years in internal medicine, and finally one to three years in the subspecialty of cardiology. 3. I think it helps to be interested in a broad range of studies and areas of life, like music, literature, helping and loving human beings in various ways. You must have courage, determination, stamina, integrity, honesty and be able to work at other jobs to earn enough money to go to school. You can not be a quitter, regardless of how tough it gets! Strive for excellence. 4. There is always competition, But I think that we can find a place for you! Just get through the training. 5. You have to love this field of medicine. You will be needed for diagnosing many problems of the heart. Very exciting is the fact that great strides in research are being made. You will be able to apply all of this knowledge, or you may want to do some of the research yourself! 6. You work hard and long hours. It is highly competitive, and it is not the most renumerative profession in the world! 7. Salary depends on where you live, how hard you work, what kind of insurance the population has etc. Range is difficult, but think like 100,0 00 to 120,000 and higher when you are well established, especially if you are an invasive, interventialist. 8. Office hours 9-12, 2-5, But it could be up to 12hours a day depending on emergencies and how hard you want to work, and whether you are in a group or alone. 9. Research, teaching, conferences 10. Such items vary and are negotiable depending on where you live etc. Hopefully, I have encouraged you to join us! RJM

E-mail received:

I wanted to thank you again. Your interview has help me understand what cardiologist do. Not many doctors take the time to e-mail someone back. You have a great heart. Thank You,

E-mail received:

I am a 30 year old male that had a tetralogy of fallot repair in 1972 in Chicago. I lived a very active childhood up through college not knowing of what was to come. In 1995 I was rushed to a hospital with sustained VT (236 bpm). I had a few EPS studies done and even an ablation done in LA there with a cardiology group under the direction of Dr. Ruggio. I am experiencing more arrythmic activity and am concerned for my future. I have a wife and 3 young children. I am currently taking 160 mg of sotalol bid and less and less rigorous activity is causing heart irregularities. What would you suggest? A defribulator or continue meds? Undergo another attempted ablation? What are my options at this point? Thank you for any advice. I don't excersice much either with what I have been experiencing.

Dr Matthews response:

In order to advise properly, I need to know what are the heart irregularities. Have you had a recent ECG and a 24hour Holter ECG to detect what these irregularities are? What do you feel with these irregularities? Are you short of breath at rest or with exertion? Do you not exercise due to fatigue and shortness of breath, or is it the irregular beating of the heart, causing symptoms of weakness, dizziness, fainting etc? Also, do you awaken during the night with shortness of breath?
When did you last have the electrophysiology studies performed? What was found?
Was the ablation initially successful?
Was the sotalol helpful initially?
Suggestions:
1.24hour Holter test to detect what is the arrhythmia at this time, correlating your symptoms with the occurrence of the irregular beats.
2.Exercise ECG with echocardiogram to elicite the arrhythmia and to check for other structural cardiac abnormalities, like a residual ventricular septal defect (repaired 29 years ago), further stenosis or leakage of the pulmonary valve.
These above conditions, if present, can cause the right side of your heart to dysfunction and lead to reduction in your exercise capacity. Of course, repair or replacement of the pulmonary valve can be accomplished if the leakage is severe.
Sometimes, an aneurysm can form at the site of the initial repair.
Some patients have recurrent obstruction of the right ventricle outflow tract, which requires repeated surgery.
Approximately 10 to 20 per cent of patients with repaired tetralogy of Fallot have residual ventricular septal defects, and such patients may require repeated surgery if the defects are of sufficient size.
3.Consider repeat electrophysiology studies, depending on the outcome of the above studies, to elicite the arrhythmia and to consider repeat ablation therapy and/or further drug therapy.
4.After number 3 above, consideration of implantable cardioverter defibrillator may be a possibility, if indeed these "irregular heart beats" are proven to be ventricular tachycardia episodes, which is not known at this time
5.Determine whether the sotalol dose is appropriate, although the 320mgs. dose is usually adequate and safer than larger doses(which can cause a special ventricular tachycardia itself).
6.Depending on what the echocardiogram shows, a heart catheterization may be necessary.
7.See your cardiologist regarding your symptoms and the above suggestions!
Please keep me advised!
Thank you for contacting me. I hope I have been of help.

E-mail received:

About 1 year ago I went to my Doctor for what was a strange feeling with my heart beat. Never had it until then. It is not really arrhythmia but may be classified as arrhythmia. I am 34 and in good physical condition. I do not smoke but drink 1-2 drinks of either beer or wine. The irregular beat starts normal and then it hesitates or pauses for a brief second, then a heavy down beat occurs. This seems to happen when I consume alcohol, but not all the time. It seems to come when there is stress as well but not as frequent as after alcohol is consumed. I also have flavored slush's that I wondered if I was allergic to. Also, my father has hypertension for which he has been on Blood Pressure meds for over 10 years (age 67). The Doctor put me on a 24 monitor and there wasn't much there. Very few irregular heavy beats.
My question is:
1) What else could be causing this?
2) Could it be an allergy? or is alcohol the main player.
3) Next steps or tests if this continues
This started up again about 1 month ago but I have not called the Doctor. He felt that it is still a normal thing and is not a danger sign (he also did a cardiogram?). Not sure what it is called but it took 15-30 seconds. It was fine.
Thanks

Dr Matthews response:

I think you may be having "premature atrial contractions", which are causing you to have palpitations(defined below).

WHAT ARE PALPITATIONS?
Palpitations is a disagreeable awareness of the heart beat,often described as a pounding, stopping, jumping, or racing in the chest.
The sensitivity of the nervous system determines whether or not the patient complains of palpitations, which are not related to the seriousness of the heart disease or the type of arrhythmia.When patients have a premature heart contraction(PACs), they feel the post-extrasystolic beat,associated with a large stroke volume,which is due to the longer filling period in diastole. A patient may be aware of a cardiac arrhythmia by detecting an uncomfortable sensation in the neck. They may complain when the heart beat is slow or fast, and when it regular or irregular.

Annoying palpitations are common symptoms of premature atrial contractions(PACs) in patients who have either no underlying heart disease or mitral valve prolapse.Reassuring the patient of the benign nature of the arrhythmia may suffice,and no therapy is necessary other than removal of the inciting factors such as cigarettes,coffee,alcohol, and excessive fatigue.When palpitations are sufficiently annoying that an intervention must be considered,a low dose of a beta-adrenergic blocking agent is preferred to more aggreessive(more dangerous)membrane-active antiarrhythmic agents.

When it is necessary to treat PACs to prevent initiation of sustained arrhythmias or because of intolerable palpitations, convential antiarrhythmic agents may be effective.Depending upon tolerance and side effects,any of the membrane-active drugs or beta-adrenergic blocking agents may be considered.

E-mail received:

I have recently found out that my mother has congestive heart failure. I have read the definitions about the disease. What I would like to know is how long can a lady of 72 life with this condition? She has had a stint put in one artery and has a defective value that may not be operated on.

Dr Matthews response:

You ask a very difficult question to answer! Whatever I write is just general information available in the literature.But you need to talk with your Mother's doctor re her specific prognosis.
The prognosis of patients with heart failure is generally poor; and in several series 50% of the patients with severe symptoms died within 12 months.In less severe heart failure,mortality approaches 50% in 3 to 4 years.The primary factor determining prognosis is the left ventricular function,as reflected in the left ventricular ejection fraction of blood being pumped out with each heat beat. Other factors that have been shown to have prognostic value include functional classification; electrolyte abnormalities such as a low sodium in the blood;elevated levels of plasma catacholamines etc;poor exercise tolerance; presence of atrial fibrillation;and coronary artery disease as the etiology of the heart failure.Many patients with heart failure, perhaps 30-40%, die suddenly,presumably from ventricular arrhythmias.Moreover,increasing heart failure is associated with an increased incidence of ventricular arrhythmias, which may be decreased by aggressive, successful therapy for heart failure or by the prevention of a low potassium or magnesium in the blood.In patients surviving myocardial infarction, the prognosis is strongly related to the ventricular ejection fraction, in addition to the amount of heart tissue (myocardium) that becomes ischemic (lack of adequate oyxgen) during stress and the amount of ventricular ectopy.
Once patients with heart failure symptoms have moderate to severe left ventricular systolic dysfunction,the mortality is quite high, averaging more than 10% per year. Studies have shown that the administration of an ACE inhibitor (captopril or enalapril) was associated with a reduction of morbid events, an apparent slowing of the progression of left ventricular dysfunction, and a trend toward a reduction in mortality.
Vasodilator therapy of mild heart failure is often appropriate in an elderly individual. The decrease in mortality with vasodilator therapy holds for the subgroup of heart failure patients over the age of 70 years.
Your Mother apparently has coronary artery disease as the cause of the heart failure. Did she have a prior heart attack (myocardial infarction)? Was the heart valve problem caused by the heart attack or was it a separat entity?

E-mail received:

I wanted to inquire about three types of medicine that my father is currently taking. The names are Protonix, Plavix, and Issosrobide. If you could possibly tell me what sort of side effects these medication can cause, I would appreciate it greatly. Thank you so much.

Dr Matthews response:

Usually the pharmacist gives the patient a brochure outlining the side effects.So you might want to check with your Father as to whether he still has the data.The list of these side effects is quite long. Hence, I can only give a few. (1) Protonix: headache, diarrhea, flatulence, abdominal pain, rash,insomnia, increased blood sugar; (2) PLavix: stomach bleeding, reduced white cell count, abdominal pain, dyspepsia, gastritis,rash; (3) isosorbide: headache, dizziness, nausea. I would advise that your Father discuss any problems with the medicines with his physician prior to stopping them.

E-mail received:

The pharmacist did not provide him with none of that info. I thank you very much for your help. Have a great day.

E-mail received:

I'm not sure if I understood this right; I've just learned that the tendon that holds the mitrial valve in place appeared to look weak in an echocardiogram. How serious is this and can it be corrected? We've been referred to a cardiologist, but that won't be until next week. I'd like to understand more.

Dr Matthews response:

The chordae tendineae are strong cords of fibrous tissue which spring from the tip of each papillary muscle in the left ventricle, attaching to the two leaflets of the mitral valve directly above. Dysfunction or rupture of a papillary muscle or rupture of a chorda tendinea may undermine the support of one or more valve leaflets, producing regurgitation of blood from the left ventricle back into the left atrium during systolic contraction, rather than flowing normally only through the aortic valve into the aorta. Such a condition can arise from coronary artery disease with ischemia or infarction, mitral valve prolapse, or rheumatic fever sequelae including scarring, left heart enlargement and dilatation from various problems like high blood pressure, hypertrophic obstructive cardiomyopathy, calcification of the mitral ring etc. Deepending on the severity of the regurgitation, surgery can correct the problem. But of course the cardiologist has to examine you and decide what needs to be done! Sincerely,Dr.Matthews

E-mail received:

Do you agree with my cardiologist that a ratio of 1.7 is borderline for surgical correction?
I am a 37 year old, non smoking male and was recently diagnosed with ASD. My Dr. ran a right heart cath and concluded my ratio was 1.7. She says any ratio under 1.5 was no cause for surgery and any ratio of 2.0 was a definite case. Thus my 1.7 is border line. I have looked through the literature on line and don't find any reference to the 1.5 to 2.0 grey area. Thanks!

Dr Matthews response:

In the New England Journal of Medicine, Jan.27, 2000,vol.342, pp.256-263, Drs.M.E.Brickner and L.D.Hillis,And R.A. Lange wrote the article "Medical Progress:Congenital Heart Disease in Adults (First of Two Parts)". With reference to surgical closure of an atrial septal defect, they advised surgery if the pulmonic/systemic blood flow ratio is approximately 1.5. This recommendation is made provided there is no serious malfunction of the left side of the heart. It is not recommended for patients with irreversible pulmonary arterial disease and high pulmonary blood pressure. Closure is recommended also for those patients with ratios of approximately 1.5, if the pulmonary artery hypertension is documented by catheterization, provided the systemic arterial saturation is approximately 92%, and the total pulmonary resistance is less than 15 Wood units (E.W.Nugent and others, The Pathology, Pathophsiology, Recognition, and Teartment ot Congenital Heart Disease, Hurst's The Heart,8th Edition.PP.1761-1771).
Of course, only your own physician and others who examine you in consultation can appropiately advise you!Dr.Matthews

E-mail received:

A family member is having a transesophogial echocardiogram. Can you explain the function of this test? How can it define any heart problems? Thank you,

Dr Matthews response:

Transesophageal echocardiography has proved to be of extreme valve and offers additional diagnostic information among patients with presumed or known prosthetic/native mitral valve dysfunction for infective endocardial lesions and their complicatins,in the assessment of intracardiac masses, in the diagnosis of thoracic aortic disease, in the detection of cardiac sources of embolus, and as an intraoperative/post operative monitoring technique among cardiac and noncardiac surgical patients (see definition echocardiography my website).Dr. Matthews

E-mail received:

Thank you for your information about the transesophogial echocardiogram. My mother had a heart attack in the 1980s and had her second stroke in May 2001and third strokes in June 2001. Both occured after her dosage of Coumadin had been reduced. One involved vision impairment and the next involved speech impairment for a period of 24 hrs. However, my mom is still weakened on her rt. side. She reports "not feeling well" though she has no specific aches or pain. She is being followed by an internist, cardiologist and neurologist. She is taking Coumadin. Her prothrombin time is about 2-2.5. She has this checked every other wk. Her latest stress test showed no further damage than what occured in the ' 80s. Her cardiologist has scheduled the esophogeal echocardiogram. Could that have to do with the risk of embolism? Thanks for your help.

Dr Matthews response:

I am very sorry about your Mother's condition!
Yes, the cardiologist will be looking for hidden blood clots in the left atrium, its appendage, and on the mitral valve (the door "so to speak" from the left atrium to the left ventricle, which sends its blood through the aortic valve to the brain. It is these blood clots, which break off and go to the brain to cause the strokes! So knowing that they are present is important for treatment and emphasizes the the risk of further embolism. I do not think the procedure itself places her at further risk though. Also, the procedure can look at the ascending aorta for evidence of ruptured, ulcerated, atherosclerotic cholesterol plaques, which can be a source of the emboli.
Does she have an irregular rhythm like atrial fibrillation, which can cause blood clots in the left atrium?
It may be that the prothrombin time (checked weekly at first) will have to run higher ( like 3.5) to prevent the recurrent emboli, inspite of the increased risk of bleeding? Of course, only her physicians can make changes etc because they have examined and know her well Dr.Matthews

Email received:

Gentlemen: it will be four weeks tomorrow that I had triple bypass surgery. How long should I wait before returning to work?I am fifty four years old and I work as a driver for UPS. My job does entail heavy lifting with an abundance of stair climbing. Thank you.....

Dr Matthews response:

Return to work is a complicated subject. Since the median age of coronary bypass patients is approaching 65 years and is older in many communities, return to full activity may be a more realistic expectation. Nonetheless, factors affecting return to work include the status of employment preoperatively, age, income, gender, self employment, whether white collar or blue collar, college education, relief of symptoms, and preoperative left ventricular function. It is known that the longer the unemployment preoperatively, the less likely the return to full employment. Other factors that adversely affect future employment include comorbidity, physician advice, and disability compensation.
It is advised that you consult with your cardiologist and consider a stress ECG test to determine your ability to run on the treadmill without symptoms and ischemia, and compare the lifting of heavy boxes to the stress on the treadmill!
Sincerely ,Dr.Matthews

E-mail received:

My husband was diagnosed with ebstein anomaly of tricuspid valve at 3 months of age. He is now 30. We have gone for regular checkups since his diagnosis. We felt he had always been asymptomatic. However he has had episodes of SVT. The doctor said he was showing a steady decline in his oxygenation, which was 88 at his last appointment, and that further investigation would be necessary. This includes the possibility of valve repair or replacement. What is your opinion and where can I find more information.

Dr Matthews response:

Ebstein's anomaly is an abnormality of the tricuspid valve in which the leaflets are abnormally developed down in the right ventricle (see attached). This abnormality allows venous blood to regurgitate from the right ventricle back up into the right atrium, and if there is a hole in the septum (a partition between the two atria, occurring in 80% of patients)into the left atrium in some of the patients. The flow of the venous blood into the left atrium is what causes the blood oxygen saturation to fall (your husband's is down to 88%, while normally it would be in the 90's). The valve may also be too narrow. The severity of the valve dysfunction with high pressure in the right ventricle is what causes the blood to go across the septum into the left atrium, leading to desaturation of the blood. The paroxysmal atrial tachcardias are also one of the complications of this anomaly and can cause cardiac failure and worsening cyanosis (desaturation) 20% of patients have ventricular preexcitation by way of an accessory pathway between the atrium and ventricle(which can cause supraventricular tachycardia like what your husband had)and is called Wolff-Parkinson-White syndrome. The treatment of the above tachcardia may be with medication or catheter ablation, radiofrequency type. Repair or replacement of the tricuspid valve in conjunction with closure of the inter atrial communication and interruption of the accessory conduction pathway (referred to above) is advised in patients with severe symptoms despite medical treament, and in patients with heart enlargement. Your husband's studies might include a color Doppler echocardiogram and an electrophysiology study to investigate respectively the tricuspid valve and the atrial septum defect, and the accessory pathway location. Of course, your own physician would know best what is needed in your husband's case. What I have tried to do is to relate some of the latest thoughts on the topic. I would appreciate keeping in touch. Dr.Matthews

E-mail received:

I am a 55 year old patient with a history of CAD. In 1998 I had a cardiac cath of a lesion RCA. I was left with an ejection of 40%. Now I had a stress test with a conclusion of mild infarct with superimposed mild ischemia. I spoke to a Cardiologist who is my friend who told me about the ACE inhibitor called altace and Vit E for in patient's with CAD but my doctor has me on Vasotec 5 mg. and 1 baby ASA, If you like I would send you my report. Are you
a Cardiologist?

Dr Matthews response:

Both altace and vasotec are ACE inhibitors, and have been shown to reduce the morality rate from congestive heart failure. I have not heard that vitamin E is similarly effective or has an action to improve the action of altace.
I think the best thing to do is to discuss the relative merits of these two drugs with your own treating cardiologist, for he knows your condition very well. I assume you are on one of the statin drugs for lowering cholesterol, as well as a low cholesterol diet.Certainly you must not smoke!
Yes, I am a cardiologist.

E-mail received:

I was recently diagnosed by an EKG as having wolff-parkinson-white syndrome. I am presently waiting for my family physician to set up an appointment with the cardiologist that comes to her office. I was not given much information at the hospital where I was diagnosed. I was told that I was probably beyond medication and would have to have an ablation procedure done.
I am a runner (age 31). I was told by my family doc that the cardiologist said I am not to run for the time being. I do not quite understand the risks involved with running as I have done so many years throughout my life. I only have a few episodes of rapid heart beats each month. I have always been able to control them with slow and deep breathing. I do sometimes have dizzy spells and
shortness of breath. I don't know that it is enoug of a reason for me to believe I am at risk when I run. I have therefore decided to run anyway. I also feel that I am pretty healthy and am under the
attitude to leave well enough alone in regard to the ablation. Any opinions or comments would be appreciated as guidance until a doc meets with me to answer some of my questions. Thanks

Dr Matthews response:

There are three choices of therapy:drugs,surgery,and catheter ablation. Patients who demonstrate a good clinical response to therapy,measured in terms of reduced frequency or rate of tachyarrhythmic episodes,can be managed noninvasively; patients with intermittent delta wave on ECG and no clinical arrhythmia need no therapy.
But patients who have frequent or poorly tolerated tachyarrhythmias, those who are prone to episodes of atrial flutter or fibrillation, or those who have a family histroy of WPW and sudden death should be evaluated by electrophysiologic testing.In such patients, catheter ablation using RF energy has emerged as the treatment of choice when available and accepted by the patient. When this is not available, surgical intervention is in order.Among those with symptomatic or life threating arrhythmias for whom such intervention are not availble or feasible, a clear cut response to antiarrhythmic treatment is mandated ( using drugs like quinidine, pronestyl, rhythmol, sotalol).
You do have only a few episodes, which are mainly mild and controlled with your deep breathing, but then you say that you get dizzy and short of breath on occasion (apparently due to rapid heart beats). Perhaps you should be monitored on a treadmill ECG test to determine if you develop a very rapid heart beat rate, which might make you prone to atrial fibrillation or flutter, which can be more serious!Also a 24 hour Holter ecg may be in order to find out more of the frequency and severity!
Sincerely,Dr. Matthews

 
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