"What Ails a Woman’s Heart" - Wallis, Scientific American Jan 2019

[MSEsperanza]

"What Ails a Woman’s Heart.
The more we look, the more we find sex differences in cardiovascular disease."

by Claudia Wallis, Scientific American Jan 2019

For years cardiologists were baffled as to why up to half of women with classic symptoms of blocked vessels—chest pain, shortness of breath and an abnormal cardiac stress test—turn out to have open arteries. Doctors called it “cardiac syndrome X.” They didn't understand it, and many women were subjected to repeated angiograms in search of blockages that weren't there.

That still happens today, but more doctors now recognize that despite having open arteries, about half of women with this pattern nonetheless have ischemia—poor blood flow through the heart. The condition has gained a mouthful of a name: ischemia and no obstructive coronary artery disease, or INOCA.

The initial mystery of INOCA was how the heart could be starving for blood if its main arteries are not blocked. The answer often lies in the smaller branches and twigs of the vascular system—arterioles and capillaries that deliver oxygen and nutrients to heart muscle. The walls of these vessels are too thin to accumulate plaque, but they can become dysfunctional, failing to contract or dilate as needed

https://www.scientificamerican.com/article/what-ails-a-womans-heart/

 

[dangermouse]

I have Microvascular Angina.

 

[MsUnderstood]

@MSEsperanza Many thanks for posting this article. It describes my situation perfectly.

Last summer, with a sibling scheduled for by-pass surgery, my physician requisitioned a nuclear stress test. I was experiencing worsening symptoms of cardiac failure, and wanted to know if it was "just ME", or yet another diagnosis to add to an already alarming list.

Even I was surprised at how difficult the stress test was. I was severely out-of-breath after less than two minutes at low-intensity, and barely made the minimum four-minute target on the treadmill. Imaging done both immediately after, and later in the day, showed ischemia. So, a CT angiogram was scheduled to determine the location of the blockages. As described in the article above, my arteries were completely clear.

My GP was baffled. However, based on a timely S4ME post ( https://www.s4me.info/threads/dr-da...nce-of-sfpn-in-some-patients.4855/#post-87219 ), I had a possible explanation. Now, several months later, details in the Scientific American article and the information provided in Doctor Systrom's interview sound the same -- the dysfunctional blood vessels failing to contract or dilate as needed, and the ventricles not relaxing enough to fill properly. Is the latter the same condition as the preload failure that is common among Doctor Systrom's ME patients? I wonder. Doctor Systrom also used the exact terminology "preserved ejection fracture" as that included in the article.

The Scientific American article raises an interesting question. Why, if this condition is so prevalent (25 - 30 percent of ischemic heart disease in women and 10 percent in men) did my cardiac evaluation end after my arteries were found to be clear? I attended the largest cardiac clinic in a large city. Weren't they aware of this?

So the good news was that I don't need by-pass surgery. For me, the potential challenges of recovery were frightening. But the bad news is also that I don't need by-pass surgery. This prospect at least provided some hope that my exercise intolerance could be improved.

One comment in the article was eerily familiar regarding the lack of therapy for Heart Failure with preserved reduced Ejection Fracture. Doctor Bairey Merz, director of the Women's Heart Center at Cedars-Sinai's Heart Institute said: "but essentially no effective therapy for HFpEF. Had we studied women 50 years ago, we wouldn't be in this situation."

Has anyone else experienced the same . . . poor blood flow through the heart with clear arteries?

 

[Arnie Pye]

The initial mystery of INOCA was how the heart could be starving for blood if its main arteries are not blocked.

Many of the usual suspects are implicated—smoking, diabetes, high blood pressure, high cholesterol—but a history of problems during pregnancy, such as elevated blood pressure and diabetes, and of depression and autoimmune diseases, both of which are more common in women, may also contribute.

My bold

I've read a few times that low blood volume is often found in autoimmune diseases which are more common in women. Another issue is that women are found to be anaemic far more than men. I'm sure this has a knock-on effect on blood volume.

Edit : This paper may be relevant to the heart starving for blood :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3226173/

Pathophysiology of fluid imbalance

Abstract
Fluid imbalance can arise due to hypovolemia, normovolemia with maldistribution of fluid, and hypervolemia. Trauma is among the most frequent causes of hypovolemia, with its often profuse attendant blood loss. Another common cause is dehydration, which primarily entails loss of plasma rather than whole blood. The consequences of hypovolemia include reduction in circulating blood volume, lower venous return and, in profound cases, arterial hypotension. Myocardial failure may result from increased myocardial oxygen demand in conjunction with reduced tissue perfusion. Finally, anerobic metabolism due to reduced perfusion may produce acidosis and, together with myocardial dysfunction, precipitate multi-organ failure. The splanchnic organs are particularly susceptible to the deleterious effects of hypotension and hypovolemic shock, and these effects, depending upon their duration and severity, may be irreversible despite restoration of normovolemia by fluid administration. Patient monitoring in the intensive care unit typically relies upon central venous pressure devices, whereas the primary focus in the operating theater is blood volume deficit estimated from suction devices. However, estimates of intraoperative blood loss can be inaccurate, potentially leading to inappropriate fluid management. Normovolemia with maldistribution of fluid can be encountered in shock-specific microcirculatory disorders secondary to hypovolemia, as well as pain and stress. Consequent vasoconstriction and reduced tissue driving pressure, as well as leukocyte and platelet adhesion, and liberation of humoral and cellular mediators, may impair or abolish blood flow in certain areas. The localized perfusion deficit may contribute to multi-organ failure. Choice of resuscitation fluid may be important in this context, since some evidence suggests that at least certain colloids might be helpful in diminishing post-ischemic microvascular leukocyte adherence. Excessive volume administration may lead to fluid overload and associated impairment of pulmonary function. However, entry of fluid into the lungs may also be facilitated by increased vascular permeability in certain pathologic conditions, especially sepsis and endotoxemia, even in the absence of substantially rising hydrostatic pressure. Another condition associated with elevated vascular permeability is systemic capillary leak syndrome. The chief goal of fluid management, based upon current understanding of the pathophysiology of fluid imbalance, should be to ensure adequate oxygen delivery by optimizing blood oxygenation, perfusion pressure, and circulating volume.

 

[MSEsperanza]

@dangermouse @MsUnderstood: I'm sorry to hear that you have to deal with these comorbidities.

@MsUnderstood : Thank you, too, for reminding me of David Systrom's findings/ hypothesis. Funnily enough, I see his study description was updated today:

https://www.clinicaltrials.gov/ct2/show/NCT03674541

@MsUnderstood @Arnie Pye :
I find all these questions highly interesting, but I'm afraid I have no clue about any of these issues. I could only add more questions. Perhaps someone who's competent in physiology will have answers. Or you could ask Dr Systrom? (His e-mail address is provided with the study description.)