Faye was clearly frustrated.
At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever.
"Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."
She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling.
But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.
A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:
--Lp(a) levels rise dramatically.
--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s.
--Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a).
All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease.
If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken.