Clinical: Case Study: Biorhythms and Arrhythmias

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Original materials created in January 1999 by Eileen Hoffman, M.D.


JL is a 43-year-old business executive with a history of recurrent palpitations. She initially presented to the emergency room for a prolonged, symptomatic episode. Her ECG showed a sustained ventricular tachycardia. Cardiology evaluation revealed multiple atrial ventricular bypass tracts. These required several endocardial ablations and antiarrhythmic therapy.

However, she remained symptomatic and eventually had an automatic implanted cardiac defribillator (AICD) placed to override and terminate these re-entrant rhythms. Due to suboptimal communication between JL and her cardiologist, she did not fully understand what life would be like with the AICD. The first time the AICD activated, JL was in an airport en route to a business trip. The electrical jolt in her chest and its physiologic reverberations sent her into a panic. She became fearful of leaving her apartment and suffered severe anxiety.

In the next several months, she experienced three more activations of the AICD. All occurred two days prior to her menses. She shared her concerns about these premenstrual episodes with her cardiologist, who laughed at her, and added sotalol (Betapace) to her regimen. On sotalol she felt fatigued and had decreased libido. Knowing that I would take her seriously, she asked for a consultation with me, a general internist and women’s health specialist.

In our visit I learned that there were no other medical issues contributing to her arrhythmia, e.g., hyperthyroidism or an electrolyte imbalance. She was not taking any herbal remedies that could act as stimulants. I referred JL to a behavioral therapist to help her with strategies to feel more in control during these AICD activations. Then I went to the library.

In fact, there was a scant, but accessible medical literature about the relationship between re-entrant tachycardias and premenstruallylower estrogen/progesterone ratios. Several arrhythmias that occur with estrogen/progesterone fluctuations have been documented in women. For example, torsades de pointes, a potentially lethal arrhythmia, is more frequent in women, and can be provoked by some common drugs, e.g., antihistamines (tefenadine and astimazole), by antibiotics (erythromycin), and even by antiarrhythmics themselves (quinidine and sotalol). By blocking potassium currents, these drugs lengthen repolarization and the QT interval. Interestingly, women NORMALLY have longer refractory periods than men, even when corrected for rate. When some women take the medications noted, repolarization and the QT interval are prolonged even further.

On follow-up with JL, I found that the sotalol had been discontinued (thank goodness!) because of her side effects and she was now on amiodarone (Cordarone), another antiarrhythmic. I contacted her cardiologist, who was unaware of the problems in prescribing sotalol to women. He felt uncomfortable “experimenting” with supplemental estrogen prior to her menses and wanted to give the amiodarone a chance. JL was uncomfortable about deviating from her cardiologist’s recommendations. She and I agreed to stay in touch.


There are many rhythmic biologic functions, e.g., seasonal, monthly, daily (circadian), or even cycles within one day (ultradian). Because the menstrual cycle is such a strong marker of time in women’s lives, many women describe physiologic events in relation to their menses, although some events, upon closer questioning, are not clearly cyclic. However, as we begin to understand the links between biorhythms, both at the organ level and at the cellular level, and the interaction between systems, e.g., neurologic, immunologic, cardiovascular, etc., the influences of ovarian steroids and/or hypothalamic factors become much more important.

Seasonal variation in light duration and intensity is associated with depression, especially in women. Asthma has not only a diurnal rhythm in its exacerbations, but in women with premenstrual asthma, a menstrual cycle-related rhythm. Premenstrual asthma is a relatively high risk condition that often leads to hospitalization and intubation. Women with temporal lobe epilepsy have an increased incidence of anovulation due to hypothalamic dysfunction. In women with seizure disorders and luteal phase progesterone deficiencies, progesterone can augment anticonvulsant therapy. Perimenopausal and premenopausal women with low estrogen/progesterone ratios can have an increased incidence of migraines that can be resolved with estrogen augmentation. Perhaps electrical conduction abnormalities are common mediators of all these phenomena related to the menstrual cycle, whether in a neuron, cardiac myocyte, or a vascular smooth muscle cell!!!

I am reminded of the elementary school rule “Stop, Look, Listen.” When we stop holding traditional medical teachings as dogma and take time to look at our patients’ data from a different perspective, i.e., their perspective, we can learn how to approach clinical problems in a woman-centered model. We need to listen to a woman’s narrative, to her report of her symptoms in the context of her life. We must be open to finding a scientifically-based validation for her experience. (Remember how dysmenorrhea was considered a neurosis before prostaglandins were discovered and myometrial contractions could be measured!)


Hara, et al, Effects of gonadal steroids on ventricular repolarization. Gender-Specific Med Digest 1998; 1:1.

Harder and Coulson, Estrogen receptors and the effects of estrogen on membrane electrical properties of coronary vascular smooth muscle. J Cell Physiol 1989; 100:375-82.

Manfredini, et al, Circadian variation in the occurrence of paroxysmal supraventricular tachycardia in clinically healthy subjects. Chronobiol Int 1994; 12:55-61.

Rosano, et al, Cyclical variation in paroxysmal supraventricular tachycardia in women. Lancet 1996 Mar 23; 347(9004):786-8.

Sarrel, Ovarian hormones and the circulation. Maturitas 1990; 12:287-98.

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