Abstract
Some of us do not work in big cities close to expert colleagues and tertiary level facilities. Living at the extremes of the country certainly can be a privilege however professional isolation is sometimes not such a great thing. At times we may struggle with complex or unusual patients. That can happen to anyone though. The point of this tale is to explain the principles I used to help a specific patient. I hope that this may assist others finding themselves in a similar clinical situation.
Very recently I have seen Melanie who is an ex-nurse who, having taken early retirement, has moved to Cornwall.
About six years ago her periods started to become erratic and she developed classical menopause symptoms of hot flushes and sleep disturbance. These were not a great bother to her at the time. She was much more concerned with breathlessness that was functionally limiting and gave rise to very reduced exercise tolerance. In a centre of excellence, she had a myocardial perfusion (MIBI) scan which was positive along with a negative coronary angiogram and was diagnosed with Cardiac Syndrome X.
I was very excited at this point in her story as I thought I understood this condition. Numerous high-level meetings for over 20 years have provided a wealth of information that may “come in handy” but is not conventionally taught. Until now I had never met anyone with a proven diagnosis. Clinical diagnosis yes but proof – no. Remember, I work in Cornwall.
My understanding is that women are more susceptible to microvascular angina than men. This affects the small vessels and is not detected in conventional angiography. In addition, their larger coronary arteries are less likely to have discrete stenotic lesions, more likely to be generally narrowed (which is difficult to pick up) and are more susceptible to vasospasm. The vasospasm is analogous to migraine and may be termed Prinz metal angina. While fewer women than men have a myocardial infarct in their 40’s and 50’s, if they do it is less likely to present with classical crushing central chest pain, can be painless and is more likely to be fatal. The risk factors of smoking and diabetes appear to have a greater relative influence in women.
Melanie’s GP knew very little of this. She had been discharged from the specialist service and had no local cardiology care. As far as he was concerned, she had clear coronary arteries. He was struggling to manage both her blood pressure and her now intrusive menopausal symptoms. He had tried clonidine which had made her feel worse but felt that hormones were out of the question. She was taking Losartan and Bendroflumethiazide. She had not tolerated betablockers, amlodipine or diltiazem. A routine series of primary care screening blood tests were normal.
Melanie was trying to work as an artist but was struggling as she could not concentrate. She had severe flushes though fewer than a year or so ago, her sleep remained disturbed, she was permanently tired, her brain fog was the most limiting symptom and she was irritable, irrational and not herself. As if that was not enough, vaginal dryness was precluding sex and causing tension at home. She had not had a period for about three years.
Although breathlessness stopped her walking and exercising it was menopause that was stopping her from working, given that her work was static. Intervention could be justified. Was HRT an option? Yes, but with reduced choice.
My stance on this was that oral oestrogen should not be considered. Having intermittent high blood pressure represents a stroke risk and the prothrombotic activity of oral oestrogen should be avoided. Non-oral oestrogen was available as an option as it does not appear to increase either DVT or stroke risks at standard dosage.
Potentially any oestrogen could have advantages to the coronary arteries via lipid metabolism effects and reduced atheroma formation. There is also some evidence of a direct vasodilation effect. At some point in the past I remember being told that oestrogen could be considered a first line treatment for cardiac syndrome X in women.
Empirically I suggested to Melanie that we could use twice weekly patches for as even a delivery dose as can be achieved. With this I suggested micronized progesterone to be taken at bed time. There is certainly data indicating that this is least likely to oppose the positive metabolic effects of oestrogen that I was looking for. The hope was that the sedative side effect profile would add to the effect of replacing oestrogen and improve sleep. This lady was certainly postmenopausal so a continuous progesterone regimen could be advised.
I explained that replacing oestrogen should reduce flushing and lift mood and her ability to concentrate. It should, but we can never promise. Accepting the poor evidence base, my advice was to start at half of the standard patch dose for a couple of weeks then titrate upwards. I was looking to avoid a sudden change that just might trigger a migraine like spasm.
So far so good. Melanie has emailed to say that the “brain fog” is lifting. I have since been in contact with her GP at his instigation and have been able to make suggestions regarding her hypertension management and further investigation. It strikes me that pulmonary hypertension might be a factor in her breathlessness that has just not been considered.
Rare things do not exclusively present to the centres of excellence: they may simply not be recognised or understood elsewhere. General practice is constrained by short appointments and great demand. Enough time to think is an advantage of a longer clinic appointment. The holistic nature of a menopause assessment offers many possible lines of help if we are sufficiently open minded to consider all the aspects presented.