Estrogen has control over the adrenaline secreted from the adrenal medulla and the adrenaline secreted from the sympathetic system.6 This control is of utmost importance during childbirth, given the effort and pain, a large amount of catecholamines are secreted, and stimulating the beta receptors can be very harmful to the integrity of the cardiac muscle.7

Calcium levels can vary throughout the month. During the premenstrual period, when there is a decrease in estrogen, there is also a decrease in calcium. In the heart, there is an enzyme, osteopontin, which protects this organ from excessive calcium deposition and directs it towards the bone system8. Estrogen controls cAMP in the entry of calcium channels to the cardiac sarcoplasm (calcium reservoir in the myocyte).9 During systole, calcium enters the myocyte through a physical phenomenon, without the need for energy. During diastole, to release calcium from a low concentration area towards the sarcoplasmic reticulum, a pump, SERCA (Sarcoplasmic Endoplasmic Reticulum Calcium ATPase), 10 and an enzyme, phospholamban, are needed to reinforce it. Both SERCA and the latter are controlled by estrogen.11 Therefore, estrogen has a critical importance in diastolic function and, along with the increase of collagen III during pregnancy, to increase cardiac output.

Mitochondria provide energy to the cardiac muscle. The mitochondrion, with glucose, fatty acids, and oxygen, produces adenosine triphosphate (ATP).12 Through fission, ATP loses a phosphate anion. This produces heat and energy. Mitochondria have the biology and morphology of a bacterium and reproduce by fission. 13 During efforts, mitochondria reproduce, depending on the heart and muscles' energy intensity.14 During pregnancy, the heart's energy need increases exponentially, so mitochondria are stimulated by estrogens to reproduce to meet energy needs. Estrogen receptors alpha and beta are found on the membranes of mitochondria, suggesting the importance of this hormone in heat and energy production. 15 It is logical to assume that the heart during pregnancy requires enormous energy to increase cardiac output by a third.

Inhypoestrogenemia, the fibroblast produces more collagen I than III,16 in the subendocardium of the left ventricle, and in the right atrium. From collagen I, fibrosis forms. 17This subendocardial fibrosis complicates diastolic relaxation. (12Increasing the heart rate increases the final diastolic pressure. (Figure 1) This hemodynamic phenomenon is reflected in dyspnea on effort, and in the case of very high frequencies, such as atrial fibrillation, can cause acute heart failure with normal cardiac contraction. In the right atrium, the fibroblast secretes collagen I , resulting in atrial fibrosis. The fibrotic right atrium is the basis for arrhythmias; And non-sustained ectopic atrial tachycardia,( Figure 2) which can evolve into limited atrial fibrillation.( Figure 3)The diastolic function is altered by the dysfunction of hypoestrogenemia in calcium metabolism.18 In the reduction of estrogen , the calsificvation of mitral annulus, aortic valve and, coronary arteries19

Estrogen has a critical function in the pump, SERCA, and phospholamban in transporting calcium to the sarcoplasmic reticulum. Therefore, this phenomenon contributes to diastolic dysfunction and an increase in final diastolic pressure 19 (Figure 1)

In extreme emotional situations, with high secretion of adrenergic substances, the myocardium is exposed to severe injuries, and due to the lack of estrogen control, it causes severe dyskinesia, which can trigger mortality. This phenomenon is called tako-tsubo, 20 occurring in 99% of women and 95% in postmenopausal women.

It is also logical to speculate that the heart of the postmenopausal woman has less cardiac energy due to hypoestrogenemia and the hormone's stimulating effect on alpha and beta receptors in the mitochondria's membrane.

Left side

5 wamen 30 to 49 years old

With angina pains

ECG inverted T waves in precordial leads

Cardiac ultrasound normal

Coronariography normal

Left diastolic pressure normal

After atropine no changes in intracavitary pressure

Intracavitary pressure suggesting severe diastolic failure

right side

10 postmenopausal wamen

with angina pains and dyspnea

with STdepression in v4.v5.v6

ultrasound signs of diastolic dysfuntion

coronariography normal

high diastolic pressure at rest

after atropine marked increase in I