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Atrial fibrillation, an arrhythmia observed more frequently in men than women, is induced by both sympathetic and parasympathetic autonomic nerve activations. The menstrual cycle in premenopausal women has been reported to modulate the autonomic nervous system: parasympathetic activity is dominant in the follicular phase and sympathetic activity is dominant in the luteal phase. However, the relationship between atrial fibrillation and the menstrual cycle has not yet been reported, because this arrhythmia is very rarely detected in premenopausal women. We experienced a 38 year-old woman with paroxysmal atrial fibrillation. Her menstrual cycle was 30.4 ± 0.5 days and the menstrual period was 3.9 ± 0.2 days for 22 cycles. Although she had taken flecainide 200 mg/day, bepridil 200 mg/day, and propranolol 20 mg/day, she sometimes experienced mild palpitations. QTc intervals measured at her visits to our clinic were 440 ± 3 msec in the follicular phase and 425 ± 2 msec in the luteal phase (P = 0.01). These changes in QTc intervals during the menstrual cycle are compatible with earlier reports. During the 22 menstrual cycles, she felt palpitations on 3.2 ± 0.7 days in the menstrual period, 6.4 ± 0.3 days in the follicular phase, and 4.1 ± 0.4 days in the luteal phase (P = 0.01). Afterward, the medication was changed from daily to periodic administration for one week beginning a couple of days before the expected menstrual time, and she did not feel symptomatic variation in her menstrual cycle. These data suggest that her symptoms related to atrial fibrillation might have been dependent on parasympathetic activity.

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A 48 year-old obese male with hypertension was admitted to our department because of severe right-dominant heart failure. His heart rhythm was 2:1 atrial flutter and the left ventricle was diffusely hypertrophic and hypokinetic. Primary aldosteronism was diagnosed based on severe hypokalemia (2.6 mEq/L) and a low renin-high aldosterone state with hypertension despite the use of an angiotensin-II receptor blocker, but its etiology could not be clarified with computed tomography, adrenal scintigraphy, and adrenal vein sampling. Ascites and edema rapidly worsened. Ascites aspiration was performed daily, until serum potassium was normalized by a full dose of an aldosterone receptor blocker (spironolactone 100 mg/day). A diuretic (furosemide) was then added. Rate control of atrial flutter was obtained with a beta-adrenergic blocker, and anticoagulation therapy was started. His heart failure was successfully controlled. Coronary arteries were normal on coronary arteriograms, and an endomyocardial biopsy sample obtained from the left ventricle did not show any specific pathological findings. Blood pressure was well controlled with the full dose of the aldosterone receptor blocker, but he died one year later due to intracerebral hemorrhage. As his heart failure was right dominant, we believe that its etiology may have been hyperaldosteronism-induced cardiomyopathy, and not advanced hypertensive heart disease.

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We experienced an 81 year-old man with heart failure and macrocytic anemia. His serum ferritin level was extremely high (> 3,000 ng/mL). Echocardiography showed a normal left ventricular (LV) ejection fraction (EF), although the total ejection isovolume index (TEI index) was markedly elevated (0.60). In a cardiac catheterization study, cardiac index, pulmonary arterial wedge pressure, LV wall motion, and coronary arteries were shown to be normal. However, atrial pacing demonstrated a negative force-frequency relationship (a decrease in arterial blood pressure with higher pacing rates). Pathological study showed hemosiderin accumulation in his liver, but not in his myocardial tissue. As earlier studies have reported that iron may play an important role in oxidative cell damage and that this ion can enter cardiomyocytes through L-type Ca(2+) channels, we started an iron chelating agent (deferoxamine) and a calcium channel blocker (verapamil) in this case. Eighteen months later, his serum ferritin levels fell significantly without any changes in anemia. The TEI index was normalized (0.21) and the atrial pacing provoked a less negative force-frequency relationship. Thus, this combination treatment may be effective in iron overload cardiomyopathy at its early stage, when LV diastolic dysfunction is dominant and LV systolic dysfunction is only latent.

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A 32 year-old woman with bilateral hilar lymphadenopathy suffered from syncopal attacks after her first delivery. Electrocardiograms showed complete atrioventricular block (AVB) and myocardial scintigrams demonstrated a decreased uptake in the anteroseptal area. She was diagnosed as having postpartal cardiac acceleration of sarcoidosis. Because she rejected permanent pacemaker implantation, we started steroid therapy under temporary pacing. Fortunately, the treatment was very effective. Even after tapering-off of the steroid, the AVB has never reappeared. Permanent pacemaker implantation with subsequent steroid therapy is generally recommended for complete AVB due to cardiac sarcoidosis. However, steroid therapy alone can be considered for some selected cases.

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Atrial fibrillation (AF) is well known to be male-dominant. Female sex hormones may be involved, since very few premenopausal women experience AF. However, a possible gender difference in older subjects has not been fully elucidated yet. We retrospectively reviewed the symptoms of 133 patients (111 males and 22 females) with paroxysmal AF (PAF) from the medical records at our hospital from 1995 to 2000, and classified the patients according to the time of the attacks as day type, night type, or unspecific type. In females, the age at the first diagnosis of PAF was significantly higher (males: 57 +/- 1 year old, females: 65 +/- 2 years old; P = 0.006) and the proportion of cases younger than 61 years old was significantly smaller (63%, 32%; P = 0.007). As in previous reports, the female group had more cases with unspecific type (26.5%, 47.6%) or with long duration (> 24 hours) (16.9%, 37.5%). In contrast to these published results, fewer women (10.5%) had frequent attacks (more than twice a week) than men (39.8%). The incidence of regular alcohol consumption, one of the most important PAF triggers, was significantly higher in men than women (84.7%, 13.6%; P < 0.0001). Even when we focused on cases older than 60 years old, the female group still had more cases with unspecific type (53.3% versus 23.1%) or with long duration (27.3% versus 14.7%) than men, and fewer with frequent attacks (0% versus 51.7%) or regular alcohol consumption (6.7% versus 82.9%; P < 0.0001) than men. The gender difference in symptoms related to PAF may depend not only on sex hormones, but also on intrinsic or social gender differences.

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It is well known that diabetes mellitus (DM) masks the cardiac symptoms during an ischemic heart attack, but there have not been reports of whether DM influences the subjective symptoms of atrial fibrillation (AF). The present study retrospectively assessed 65 patients who were revealed to be in sinus rhythm at their first visit to hospital and who had experienced episodes of AF (or paroxysmal AF) during the follow-up period. Compared with non-DM cases (n=50), DM patients (n=15) had a tendency to a more rapid heart rate in sinus rhythm (73+/-4 vs 66+/-2, p=0.07) and higher averaged ventricular response at the first-recorded episode of AF (111+/-7 vs 99+/-3, p=0.10). However, the ratio of symptomatic cases at first-recorded AF tended to be lower in DM cases (33% vs 58%, p=0.08). When patients with beta-blockers or other antiarrhythmic agents were excluded, the ratio of symptomatic patients at first-recorded AF was significantly lower in the DM cases (25% vs 61%, p=0.04), although there was not a significant difference in averaged ventricular response at first-recorded AF (112+/-8 vs 106+/-5). The prevalence of DM neuropathy was significantly higher in asymptomatic patients (70% vs 0%, p=0.01). DM may mask the cardiac symptoms of the first-recorded episode of AF, possibly because of DM neuropathy.

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A 75-year-old man had a 26-year history of hypertension and an 18-year history of effort angina pectoris. He suffered acute myocardial infarction at age 61. According to serial echocardiography, the initially hypokinetic segment of the left ventricular apex was transformed to an apical aneurysm over the course of 10 years (at age 71). Ten months later, a transient ischemic attack occurred, despite the administration of aspirin. At age 72, echocardiography revealed a hyperechoic lesion that was suspected to be a thrombus within the aneurysmal cavity. Cerebral infarction (right occipital lobe) occurred 13 years after myocardial infarction, at age 73. After warfarin therapy for 3 months, the thrombus-like echo in the left ventricular aneurysm disappeared.

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FK506 binding proteins (FKBPs 12 and 12.6) interact with ryanodine receptor (RyR) and modulate its functions. FK506 binds to and reverses effects of FKBP on RyR, thus increasing RyR sensitivity to Ca2+, decreasing RyR cooperativity, and increasing RyR open probability. FK506 would thus be expected to have an effect on excitation-contraction coupling, but which of these FK506 effects predominates and how the [Ca2+]i transient would be altered are difficult to predict. FK506 has been reported to increase the [Ca2+]i transient in rat myocytes, but effects in other species have not been described. We compared the effects of FK506 on [Ca2+]i transients, L-type Ca2+ channel and Na/Ca exchange currents, membrane potential, and sarcoplasmic reticulum (SR) Ca2+ content in adult mouse and rabbit ventricular myocytes (VM). FK506 (10 microM) increased the [Ca2+]i transient in mouse VM (656 +/- 116 to 945 +/- 144 nM, p < 0.001) but decreased the amplitude of [Ca2+]i transients in rabbit VM (627 +/- 61 to 401 +/- 37 nM, p < 0.001). Similar effects were observed with rapamycin. The effects of FK506 and rapamycin on [Ca2+]i transients in VM of both species were reversible upon washout. FK506 did not alter SR Ca2+ content in mouse VM (0.79 +/- 0.1 versus 0.78 +/- 0.1 pC/pF) but reduced the SR Ca2+ content in rabbit VM (0.43 +/- 0.05 versus 0.30 +/- 0.04 pC/pF, P < 0.05) [pC = the integral (pA. s) of the caffeine-induced inward I(Na/Ca) normalized by cell capacitance (pF)]. FK506 had no effects on membrane potential, I(Ca,L) and outward I(Na/Ca) in either mouse or rabbit VM. These results indicate that alteration of the functions of RyR by FK506-mediated dissociation of FKBP from RyR has different species-dependent effects on SR Ca2+ load and thus [Ca2+]i transients. This difference may result from the fact that [Na+]i is low in rabbit myocytes, allowing extrusion by Na+/Ca2+ exchange of Ca2+ released by FK506-induced dissociation of FKBP12.6 from SR RyR.

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