Alterations In Cycle Length Research Articles

Hubungan Antara Kadar Hormon Dengan Perdarahan Di Luar Siklus Menstruasi Pada Wanita Usia Subur

Bleeding disorders outside the menstrual cycle are reproductive system disorders commonly experienced by women during their reproductive years. These disorders are characterized by changes in menstrual periods, including alterations in cycle length, duration of menstruation, or volume of bleeding, with a worldwide prevalence ranging from 3% to 30%. Hormonal factors are often implicated as causes of bleeding disorders outside the menstrual cycle. Preliminary findings from a study conducted at RSIA Puri revealed that three female patients seeking treatment experienced bleeding disorders outside the menstrual cycle, with two of them exhibiting low estrogen levels (below 20 pg/ml) upon examination. The purpose of this study was to analyze the relationship between hormone levels, particularly estrogen, and bleeding outside the menstrual cycle in women of childbearing age at RSIA Puri Malang. The research employed a quantitative analysis through a cross-sectional approach. Primary and secondary data were obtained from laboratory examinations of estrogen levels in blood serum on the third day of menstruation. The sample consisted of 34 mothers who met the criteria of experiencing menstrual disorders and visited RSIA Puri Malang, and who willingly participated as respondents, selected through quota sampling. Data analysis was conducted using the Chi-square test, and the results revealed a significant relationship between estrogen levels and bleeding outside the menstrual cycle, or metrorrhagia (p-value = 0.018; OR = 0.107). This suggests that estrogen hormone regulation plays a crucial role in preventing menstrual irregularities. In conclusion, maintaining optimal estrogen hormone levels is essential for preventing and managing menstrual irregularities and bleeding disorders outside the menstrual cycle.

Menstrual cycle, sex hormones in female inflammatory bowel disease patients with and without surgery.

Healthy women at reproductive age experience a cyclical alteration of gastrointestinal (GI) symptomatology during their menstrual cycle. Additionally, the majority of healthy women also complain of worsening of GI symptoms either during the premenstrual or menstrual phase. Despite conflicting evidence, studies suggest that sex hormones may increase GI transit time during the luteal phase. Similar phenomenon is also observed in women with underlying inflammatory bowel disease (IBD). The mechanism underlying this complex pathophysiology is still not completely understood. However, a possible influence of sex hormones on the brain-gut-microbiota axis is hypothesized. The diagnosis of IBD is associated with a delay in menarche as well as menstrual function irregularities including alterations in cycle length and the duration of flow. There is little data on the effect of menopause on IBD disease activity and conflicting data on the effect of IBD diagnosis on the onset of menopause. The role of contraceptives and hormone replacement therapies on the development or disease activity of IBD has not been yet established. Moreover, IBD patients with concomitant dysmenorrhea report heightened pain during menses. The effect of non-steroidal anti-inflammatory drugs in treating primary dysmenorrhea on the disease course of IBD is unknown. In addition, the effect of IBD medications including immunomodulators and biologics on menstrual function remains unclear. Also, the role of IBD surgery on menstrual irregularities needs to be fully elucidated. Hence, understanding the influence of menstrual function on IBD disease activity and vice versa and the maintenance of normal menstrual function in those patients is important in improving overall reproductive health and fertility and outcome of IBD.

Poincaré plots and tachograms reveal beat patterning in sick sinus syndrome with supraventricular tachycardia and varying AV nodal block

Using 24-h ambulatory electrocardiography, the RR intervals of all beats were determined in a West Highland white terrier with sick sinus syndrome characterized by long sinus pauses, bradycardia, supraventricular tachycardia (SVT) and varying degrees of atrioventricular (AV) heart block. Distinctive patterns of bradycardia and 1:1, 2:1, 3:1, 4:1 and 5:1 AV block associated with SVT were evident in the tachogram (RR interval distribution over time) and Poincaré plots (short-term heart rate variability plots of RRn versus RRn + 1). These patterns differed from those of abrupt alteration in cycle length during long sinus pauses or bursts of supraventricular tachycardia. Recognition of such patterns may direct attention to time points for which close attention to the cardiac rhythm should be evaluated in the full-disclosure of the 24-h ECG recording.

Human ventricular action potential duration during short and long cycles. Rapid modulation by ischemia.

Mechanisms underlying the initiation of ventricular arrhythmias in ischemia by a premature beat or after a pause remain unclear. The kinetics of electrical restitution, which is the modulation of action potential duration (APD) by an abrupt alteration in cycle length, may be important. We recorded one or two simultaneous monophasic action potentials (MAPs) from the right ventricular septum during balloon occlusion of the left anterior descending coronary artery (LAD) (14 patients), which is expected to induce ischemia at the recording site, and during occlusion of the right coronary artery (RCA) (7 patients), which is not expected to induce ischemia at the recording area. The latter acted as a control. A test pulse sequence was incorporated whereby during steady-state pacing, test beats of altered cycle length were interpose. During LAD occlusion, APD for basic beats shortened from 260 +/- 4 to 236 +/- 4 ms (P < .0001), whereas the control group (RCA occlusion) showed no significant change (251 +/- 7 to 249 +/- 9 ms; P = NS). LAD occlusion resulted in flattening of the slope relating APD of test beats to diastolic interval (P = .001), whereas in the control group (RCA occlusion) the slope remained unchanged. Similar results were obtained during a second occlusion. LAD occlusion in patients during balloon angioplasty shortened MAP duration of basic beats and minimized, abolished, or reversed the normal APD/diastolic-interval relation of test beats of altered cycle length at sites served by the occluded vessel. The results suggest that ischemia flattens the electrical restitution curve in the human endocardium. These findings may have important implications in arrhythmogenesis.

Linearity of pulsatile pressure-flow relations in the embryonic chick vascular system.

The calculation and modeling of vascular input impedance are based on the assumption that pressure and flow are linearly related in the frequency domain. However, this assumption has not been proven for the embryonic circulation. Therefore, we investigated the linearity of pulsatile pressure flow relations in vivo with acute alterations in cycle length. We simultaneously measured dorsal aortic pressure with a servonull system and flow velocity with a 20-MHz pulsed-Doppler system in stage 24 chick embryos (n = 38). Cycle length was acutely altered using thermal probe(s) applied to the sinus venosus. We determined the impedance spectra at several cycle lengths for each embryo and a reference curve from a three-element Windkessel model with the use of nonlinear curve fitting. We then assessed the scatter of experimental impedance along the reference curve as a measure of linearity in the frequency domain. We found that mean vascular resistance did not change after thermal probe applications (P > .20 for each), indicating that acute alterations in cycle length did not alter peripheral vascular properties. Superpositioned impedance spectra showed minimal scatter along the model impedance from 0 to 6 Hz. Goodness of fit values (R2) were near unity (.94 to .97) and were similar for all interventions (P > .07 for Fisher's z, by F test). Above 6 Hz, both modulus and phase spectra exhibited significant scatter (P < .05, by F test). Experimental impedance spectra tended to have a fluctuation and a phase-zero crossover, indicating significant wave reflection in the embryonic circulation. Thus, the embryonic vascular system can be approximated as a linear system from 0 to 6 Hz, the range in which the majority (96.0 +/- 0.18%) of hydraulic energy is dissipated.

Pharmacologic alterations in human type I atrial flutter cycle length and monophasic action potential duration Evidence of a fully excitable gap in the reentrant circuit

Objectives. This study compared the effect of change in action potential duration versus conduction velocity on atrial flutter cycle length to determine whether there is a fully or partially excitable gap in atrial flutter.Background. In an excitable gap reentrant circuit, cycle length is proportional to conduction velocity. Action potential duration is not a direct determinant of cycle length when the gap is fully excitable.Methods. Right atrial monophasic action potentials were recorded from 41 patients during type I atrial flutter before and during pharmacologic interventions.Results. Adenosine *17 ± 3 mg [mean ± SD] shortened (p < 0.001) action potential duration but did not change cycle length. Edrophonium (10 mg) had no significant effect on action potential duration or cycle length. Isoproterenol (0.03 μg/kg body weight per min) shortened (p < 0.05) and procainamide (15 mg/kg, then 2 mg/min) prolonged (p < 0.001) action potential duration and cycle length. Alterations in cycle length were not correlated with changes in action potential duration. Procainamide's prolongation of action potential duration was reversed by adenosine without affecting cycle length. Procainamide's prolongation of action potential duration and cycle length was partially reversed by isoproterenol. Adenosine's and isoproterenol's shortening of action potential duration and isoproterenol's shortening of cycle length were enhanced by procainamide.Conclusion. Atrial flutter cycle length is determined primarily by conduction velocity and does not depend directly on action potential duration. Atrial flutter has a fully excitable gap, and procainamide does not convert the gap from full to partial excitability. Adenosine and isoproterenol interact with procainamide such that their effects are enhanced and procainamide's effects are diminished.

Influence of acute alterations in cycle length on ventricular function in chick embryos.

Heart rate (HR), developed pressure, and stroke volume (SV) increase dramatically during cardiac morphogenesis. During acute changes in cycle length (CL), the chick embryo maintains cardiac output by a compensatory change in SV. We determined embryonic pressure-volume relations during alterations in CL in the stage 21 while Leghorn chick embryo to quantitate the relationship between CL and cardiac time intervals, ventricular preload, and ventricular function. CL was transiently altered to 73-191% of initial baseline CL with a 1-mm randomly preheated or cooled metal probe applied to the sinus venosus. Isometric relaxation, diastolic filling, and systolic ejection times varied linearly with CL, whereas isometric contraction times were similar. SV varied linearly with CL, ejection time, and end-diastolic volume. In contrast to the mature heart, the relationship between SV and end-systolic pressure was inverse. Embryonic ventricular preload was influenced acutely by diastolic filling time, and cardiac output was optimized during changes in CL by ventricular-vascular interactions that matched SV inversely to HR.

The interrelation between the monophasic action potential duration, cycle length and ischaemia in the human left ventricle.

Steady state monophasic action potentials were recorded from a single site in the left ventricular endocardium during incremental atrial pacing to the point of angina in 25 patients. Ischaemic areas of the left ventricle were documented using a perfusion marker (99mTc-MIBI) simultaneously with the action potential recording procedure. Recordings were obtained from an ischaemic area in 13 patients and from a non-ischaemic area in 12. A linear correlation between action potential duration and cycle length changes was demonstrated for both ischaemic and non-ischaemic zone recordings between cycle length changes of 750 and 428 ms. Ischaemia induced a shortening of the action potential duration significantly greater than that produced by cycle length changes (P less than 0.0001). Mean action potential duration shortening corrected for 100 ms change in cycle length for ischaemic zone recordings was 31.4 +/- 4.2 (SD) compared to 23.3 +/- 3.1 ms for non-ischaemic zone recordings. A range of values of action potential duration shortening in unit time was analysed for sensitivity and specificity for the detection of ischaemia. A value of 26.5 ms per 100 ms change in cycle length provided the optimum compromise with 88% sensitivity and specificity. Our data provide a means of employing the monophasic action potential duration to quantify early localized ischaemia in the presence of an alteration in cycle length.

Luteal-phase defect induced by deprivation of FSH at a specific period of the follicular phase prevents pregnancy in the bonnet monkey (Macaca radiata)

Female bonnet monkeys were injected i.v. with 25 microliters antiserum to FSH on Days 5, 6 or 7 of the cycle: the length of the luteal phase was shortened but there was no alteration in cycle length. Proven fertile females (N = 6) were caged throughout the period of the experiment (6 cycles) with proven fertile males and treated with 25 microliters FSH antiserum on Day 7 of each of 3 successive cycles. Out of 18 cycle exposures during the treatment phase, 17 were ovulatory, but no pregnancies occurred. In the post-treatment phase, 5 monkeys became pregnant within 3 cycle exposures. These results show that it is possible to render female monkeys infertile by creating luteal insufficiency and this can be achieved repeatedly in a reproducible manner by depriving the cyclic females of FSH support on Day 7 of consecutive cycles.

The Tall R Wave in Lead V1 in Posterior Myocardial Infarction: A Reciprocal Sign or a His‐Purkinje Conduction Disturbance?

The significance of the tall R wave in lead V1 with an R/S ratio greater than or equal to 1 in posterior myocardial infarction (PMI) was investigated in 28 patients during programmed electrical stimulation. The patients had been admitted with acute PMI documented by electrocardiogram and proven by enzymatic increase. Electrophysiological study was performed 3 weeks after acute PMI. In 17 of the 28 patients (group 1), the tall R wave in V1 disappeared during stimulation: In 13 of them a premature atrial extrastimulus was responsible for an abrupt normalization of QRS complex in V1 related to an increase in AH or HV interval. In the 4 remaining patients the disappearance of the tall R wave in V1 was related to a sinus pause. In 14 patients of group 1, a different prematurity in atrial stimulation induced a right or left bundle branch block (BBB). In 11 of the 28 patients (group 2) the tall R wave in V1 was unchanged but a premature atrial extrastimulus induced a right BBB in 5 patients and a left BBB in 6. In conclusion, the normalization of QRS complex in lead V1 during atrial stimulation or alterations in cycle length suggests that the tall R wave in V1 in PMI is not a simple reciprocal sign of leads V8 V9. Its association with different varieties of BBB and changes in AH or HV intervals could suggest a relationship with a His-Purkinje conduction disturbance in some patients.

Differential Effects of Abrupt Cycle Length Changes on the Refractoriness of Accessory Pathway, His‐Purkinje System, Atrial and Ventricular Myocardium in Wolff‐Parkinson‐White Syndrome

We compared the response of the accessory pathway (AP), the atrial myocardium, the His-Purkinje system (HPS) and the ventricular myocardium during steady state (constant cycle length) and following an abrupt alteration in cycle length in 23 patients with Wolff-Parkinson-White syndrome. The durations of the anterograde and retrograde refractory periods were measured during constant drive cycle lengths of 600 and 400 ms (Method I) and during an abrupt change in cycle length of either short-to-long (400 to 600 ms) (Method II) or long-to-short (600 to 400 ms) (Method III) just before the extra stimulus. The mean durations of the anterograde effective refractory periods of the APs were 295 +/- 43, 243 +/- 39 and 273 +/- 37 ms at 600, 400 and 400 to 600 ms cycle lengths, respectively. For the atrial effective refractory periods at the three cycles, they were 238 +/- 18, 217 +/- 11 and 241 +/- 17 ms, respectively. During ventricular stimulation, the mean durations of the retrograde effective refractory periods of the APs were 263 +/- 25, 245 +/- 19 and 253 +/- 21 ms at cycle lengths of 600, 400 and 400 to 600 ms, respectively. For the relative refractory periods of the HPS, they were 335 +/- 29, 239 +/- 23 and 367 +/- 38 ms, respectively and, for the effective refractory periods of the ventricular myocardium, they were 227 +/- 17, 206 +/- 15 and 215 +/- 18 ms, respectively. The retrograde effective refractory period of the HPS could be measured in only five patients at the three cycles (600, 400 and 400 to 600 ms) and the mean values were 265 +/- 57, 225 +/- 14 and 305 +/- 27 ms, respectively. With Method III, AP and ventricular myocardium responded in a cumulative manner while HPS demonstrated paradoxical effect. Compared to Method I, changes with Methods II and III were statistically significant for all variables measured. During all three cycles, the retrograde effective refractory period of the HPS exceeded the effective refractory period of the AP; and the HPS demonstrated progressive conduction delay while the AP responded to no or minimal delays when the V1V2 intervals were similar. An abrupt cycle length change of the short-to-long type facilitated the induction of orthodromic tachycardia during ventricular pacing.(ABSTRACT TRUNCATED AT 400 WORDS)

Sex Hormones in the Aging Female

Aging of the human ovary results in a gradual diminution in ovarian steroid production, followed by an abrupt and almost complete cessation of both estrogen and progesterone production at the menopause. Although carefully controlled quantitative studies have not been published, it appears that the human reproductive axis still retains its ability to respond to steroid action. However, it still remains to be determined if alterations in cycle length and regularity preceding the menopause are due to changes in ovarian function or to subtle changes in the hypothalamic pituitary axis. More experimental evidence is available to describe the etiology of age-related reproductive dysfunction in laboratory rodents. From these studies, it appears that hypothalamic dysfunction is the principal cause for cessation of reproductive cycles. Recent evidence suggests that aging of the hypothalamus is due to cumulative effects of estrogen exposure over the course of the reproductive life span.

Prostaglandin E (sulproston) is neither luteolytic nor luteotrophic during the estrous cycle in the pig

Prostaglandin E 2 (Sulproston, S) can induce parturotion and luteolysis during late pregnancy in the pig. We now tested whether Sulproston is able to interfere with the duration of the pig's estrous cycle. Sulproston was given i.m. in two injections (0.008 mg/kg each) at 12-hour-intervals to ten gilts day 10, to five gilts day 14 and to five gilts day 16 of the estrous cycle. Blood was collected shortly before and up to 48 hrs after the onset of treatment; further daily blood samples were taken from a day 0 (1st day of standing heat) to the end of the cycle. Sulproston-administration did not shorten or lenghten the duration of the estrous cycle, nor were plasma-progesterone levels altered when compared to controls. In a second study five gilts received the tenfold amount in plasma-progesterone (8.52 ± 2.8 SEM ng, treatment vs. 32.95 ± 1.86 SEM ng/ml, control) occurred on day 11, which had returned by day 16 to the level of controls (19.22 ± 6.28 ng/ml vs. 26.75 ± 2.10 SEM ng/ml, respectively). No alteration in cycle length occurred. Therefore the PGE 2-analogue Sulproston - though luteolytic in late pregnancy - is neither luteolytic nor luteotrophic during the estrous cycle of the pig.