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borderline mitral valve prolapse with mild tricuspid regurgitation
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borderline mitral valve prolapse with mild tricuspid regurgitation

Hello, I have recently undergone a nuclear treadmill stress test, a EKG and an echo and found out I have a borderline mitral valve prolapse with mild tricuspid regurgitation.  I am very worried about this.  I am a 35 yr old female and this came on all of a sudden.  One day I had a near faithing spell with a very rapid heart rate, later I went to the ER and they found nothing there, but my regular DR. called for the stress tests etc.  I had a rapid heart beat attack during the resting portion of the stress test and my heart rate went to 146.  I have not felt well for over a week now.  My Dr told me to take zanax every 6 hrs to stop any panic attacks.  I have been referred to a cardiologist and was wondering on a scale of 1 to 10 how severe this problem is, long term.  Is it manageable, and do you have to take meds for the rest of your life? Are there any limits with this condition, things to avoid etc... Will the rapid heart beat ever stop?  I have just been feeling weak with a headache and have a loss of appetite.  Could be the stress I guess, but was wondering if anyone here has this and how they deal with it, and what I should ask/tell the cardiologist when I see him.  Thanks for any and all advice.
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612876 tn?1355518095
After having that rapid heart rate, the question now should probably be whether it is POTS which is characterized by rapid heart rate (under certain conditions).  The test to ask for to rule out POTS (postural orthostatic tachycardia syndrome) is a tilt table test, and you can ask the cardiologist about this.  Not all doctors are knowledgeable about dysautonomia and POTS, so if this particular doctor isn't, don't be afraid to seek out one who is (most patients end up heading for a major teaching hospital).  POTS is frequently misdiagnosed as panic attacks; I mention this because you are being treated with xanax, presumably for anxiety, despite the fact that they have already identified some cardiac involvement (typical in cases of dysautonomia).

As for how severe the problem is (dysautonomia in general), it varies widely by person.  Some people make a complete recovery; some progressively worsen over time and are severely disabled by the condition.  Different types have different prognoses, but even within one type of dysautonomia there may be wide variance.  Take POTS, for example.  In a 2006 article, "The Postural Tachycardia Syndrome" by Drs. Blair Grubb (one of the most renowned specialists), Yousuf Kanjwal, and Daniel Kosinski a rating system is proposed to quantify the severity of orthostatic intolerance "(similar to that for heart failure)."  Grade 0 is normal.  Grade III is "Orthostatic symptoms develop on most occasions and are regularly unmasked by orthostatic stresses.  Subject is able to stand for >1 minute on most occasions.  Patient is seriously incapacitated, being bed- or wheelchair-bound because of orthostatic intolerance.  Syncope/presyncope is common if patient attempts to stand."  

As you can see, at its most severe, POTS can render a person bedridden and cause them to faint most of the time if they attempt to stand up; obviously it can be very severe.  But on the other hand, some people may have it and never once faint except under the contrived conditions of the tilt table test or maybe not even then.  Their elevated heart rate may stay within certain limits and in normal sinus rhythm, such that it is an occasional discomfort or annoyance, but otherwise benign.  And they may completely recover from the condition within a number of years.  It depends on the cause of their POTS, which form of POTS they have, and perhaps other factors.

I suppose I am giving you a lot more gray area, rather than answering your questions.  Perhaps once your doctor runs more tests and knows more about your particular case, they can give you an educated guess about your prognosis.  
Avatar f tn
I have the exact conditions you have with regard to the same 2 valves and do not have symptoms of POTS. I do have many other symptoms, some of which increase and decrease with the heart symptoms. The worst thing you can do is to allow the label of panic attacks. If you ever have a true emergency that makes the heart symptoms worse or is made worse by a poorly functioning heart, the last thing you want is a record that suggests there's nothing wrong with you except a history of panic attacks.

Tricuspid valve insufficiency is not often addressed and usually dismissed by doctors, but I'm not willing to rule out the potential seriousness of it, especially when combined with mitral insufficiency as well. My heart symptoms become worse when I have what would normally be considered local infections, with heat and humidity and other stressors. I've had some improvement since starting to use digestive enzymes, but haven't stressed myself enough to truly test how much that's helping. I began using them because my amino acid lab results didn't reflect my dietary protein intake, suggesting a malabsorption problem.

I experience PH, pleural effusion, and chronic swelling throughout my legs and feet, and hands too at times. I'm not certain the swelling is from this, as it acts more like lymphedema (if that's different) and because I have other symptoms suggestive of a chronic, sub-clinical infection. I've had a tendency to palpitations/pounding pulse/awareness of heartbeat on waking, mild shortness of breath and sudden weakness/fatigue, being too exhaused to speak at times.

I'm sorry I failed to save the references from which I got these notes but here's a little information to start with that might be of some use. Incidentally, I never had any of the so-called risk factors listed, but did have exposure to infections and heavy metals that I consider to be possible risk factors.:

Triscuspid insufficiency & Right ventricle failure

Although congenital causes of tricuspid insufficiency exist, most cases are due to dilation of the right ventricle. Such dilation leads to derangement of the normal anatomy and mechanics of the tricuspid valve and the muscles governing its proper function. The result is incompetence of the tricuspid valve. Common causes of right ventricular dilation include left heart failure, pulmonary hypertension, and right ventricular infarction. One notable exception to right ventricular dilation as a cause of tricuspid insufficiency occurs in right-sided endocarditis (i.e. infection affecting the right side of the heart). In that case, there is direct damage to the tricuspid valve as a result of infection.

Symptoms and Signs
Tricuspid insufficiency may be asymptomatic, especially if right ventricular function is well preserved. Conversely, edema, vague upper abdominal discomfort (from a congested liver), and fatigue (due to diminished cardiac output) can all be present to some degree. On examination, the jugular venous pressure is usually elevated, and 'CV' waves can be seen. The liver may be enlarged and is often pulsatile (the latter finding being virtually diagnostic of tricuspid insufficiency). Peripheral edema is often found. In severe cases, there may be ascites and even cirrhosis (so-called 'cardiac cirrhosis).


Right ventricular failure medical dictionary

Any weakening of the right ventricle that results in the back up of blood in the venous system, liver, gastrointestinal tract and extremities. The causes of this condition include left-sided congestive heart failure, emphysema, valvular heart disease, cardiomyopathy, anaemia, hyperthyroidism, cor pulmonale and congenital heart disease. Risk factors include diabetes, alcoholism, obesity and smoking.

Symptoms include swelling of the feet and ankles, nocturia, increased distention of neck veins, fatigue, weakness and fainting, Ascites, arrhythmias and pleural effusions are complications of right ventricular failure.


Right ventricular failure

Leo G. Kevin and Matthew Barnard
University Department of Anaesthesia, National University of Ireland Galway Ireland,                     Department of Anaesthesia, The Heart Hospital, University College London Hospitals


Whilst failure of the left ventricle (LV) has been the subject of intense interest for decades, failure of the right ventricle (RV) has tended to receive scant attention. Indeed, the RV was long considered a relatively passive conduit for blood flow between the systemic and pulmonary circulations.

More recently, the importance of the RV in maintaining haemodynamic stability and organ function has been recognized. It is now known that RV failure is not only as common as LV failure, but also that isolated RV failure may carry a worse prognosis than isolated LV failure. RV failure presents unique challenges in identification and management. Therefore, for an anaesthetist, a good understanding of both RV physiology and the impact of RV dysfunction is essential in order to safely manage these potentially complex patients. This review aims to provide a broad overview of RV physiology and of the pathophysiology of RV failure. General haemodynamic aims and specific therapies will be discussed.



Tricuspid valve insufficiency/regurgitation

Tricuspid regurgitation is a disorder involving backward flow of blood across the tricuspid valve which separates the right ventricle (lower heart chamber) from the right atrium (upper heart chamber).

This occurs during contraction of the right ventricle and is caused by damage to the tricuspid heart valve or enlargement of the right ventricle.  

The most common cause of tricuspid regurgitation is not damage to the valve itself, but enlargement of the right ventricle, which may be a complication of any disorder that causes failure of the right ventricle.

Other diseases can directly affect the tricuspid valve. The most common of these is rheumatic fever, which is a complication of untreated strep throat infections. The valve fails to close properly, and blood can flow back to the right atrium from the right ventricle, and from there back into the veins. This reduces the flow of blood forward into the lungs. The condition affects about 4 out of 100,000 people.
Avatar n tn
I  am 61 years old and was born with mitrovalve prolapse and tachycardia.  As a child going to school I would have an attack of tachycardia (my heart would beat 196beats a minute) and I thought I was dieing because as soon as it started it felt like my heart was turning over and over and I felt I could not get my breath.  Things that seamed to trigger it was eating citrus, playing hard, bending over, eating sweets, getting upset or anxious about something, or waiting too long to eat or eating too much.  Any of these could start the tachycardia.  As I got older I married and had 2 children ...Still had it but not as often. When I started going thru the change of life I got worse again.  Then I started hormones and got better .  Now I am haveing an attack about every month or less.  I just don't know what to do about it.
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