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Biomedical subjects

N el-Sherif

Publications and source records attributed to N el-Sherif.

At least 73 records · Page 4Linked to original sources
PubMed1991

The effects of labetalol and prazosin on exercise haemodynamics in hypertensive patients.

The antihypertensive and haemodynamic effects of labetalol were compared with those of prazosin both at rest and during bicycle exercise in 38 moderate to moderately severe hypertensive patients (supine DBP 95 to 119 mmHg when untreated). Following a two week open placebo phase to establish baseline BP and baseline exercise performance, patients were randomly and double-blindedly assigned to receive labetalol or prazosin. Drug dose was titrated from 100 to 400 mg labetalol twice daily, or from one to 10 mg prazosin twice daily at weekly intervals until BP was controlled (supine DBP less than or equal to 90 mmHg with at least a 10 mmHg decrease from baseline). Eighteen labetalol and twenty prazosin patients achieved BP control and were subsequently reexercised to fatigue on a bicycle ergometer. The mean changes from baseline for heart rate and rate pressure product (heart rate x SBP) were reduced only in the labetalol group; the difference between the labetalol and prazosin groups was significant (P less than 0.01) both at rest and during exercise. This haemodynamic profile of labetalol may be important in selecting a vasodilating antihypertensive for patients with concomitant ischaemic heart disease.

Adult↗
PubMed1990

Effects of exercise on the signal-averaged electrocardiogram in coronary artery disease.

The effects of exercise on the signal-averaged electrocardiogram (SAECG) were investigated in 52 patients with stable coronary artery disease. The SAECG was recorded before and immediately after the exercise test and analyzed at 25 to 250 Hz and 40 to 250 Hz. All patients had SAECG with noise level less than or equal 0.8 microV at 25 Hz and less than or equal to 0.6 microV at 40 Hz and with the difference in noise level between control SAECGs and SAECGs after exercise less than or equal to 0.2 to 0.3 microV. Twenty-eight patients developed ST changes consistent with transient subendocardial ischemia that persisted during the SAECG recording after exercise. There was no significant difference between control SAECGs and SAECGs after exercise in patients with or without a positive exercise test. The absence of significant change on the SAECG was not related to the presence or absence of prior myocardial infarction, site of infarction, development of exercise-induced ventricular arrhythmias or presence of an abnormal recording at baseline. These data suggest that exercise-induced electrophysiologic changes and ventricular arrhythmias may not be related to the anatomic-electrophysiologic substrate that underlies late potentials on the SAECG.

Arrhythmias, Cardiac↗
PubMed1990

Use of heart rate spectral analysis to study the effects of calcium channel blockers on sympathetic activity after myocardial infarction.

We used spectral analysis of heart rate variability (HRV) to study the effects of the calcium channel blockers diltiazem and nifedipine and the beta-blocker metoprolol on the sympathetic nervous system in patients following myocardial infarction. Energy in the low-frequency range (0.04 to 0.12 Hz) in the standing (tilt) position was used as a quantitative index of sympathetic activity. Twenty-seven male patients, mean age 62 +/- 13 years, were studied 2 to 6 weeks after myocardial infarction. Eight patients received metoprolol, 100 mg twice daily; nine patients received diltiazem, 60 mg three times daily; and 10 patients received nifedipine, 10 mg three times daily. HRV and arterial blood pressure were recorded before and 5 to 7 days after initiation of therapy. None of the drugs had significant effects on the systolic blood pressure, and only nifedipine significantly reduced the diastolic blood pressure. Metoprolol and diltiazem reduced the low-frequency HRV in all patients studied, but nifedipine had no consistent effects. Our results suggest that diltiazem had a depressant effect on sympathetic activity similar to beta-adrenergic blockers. This effect was not observed with nifedipine. The reduction in sympathetic activity by diltiazem may contribute to its therapeutic effects in the post-infarction period.

Adult↗
PubMed1990

Reentrant ventricular arrhythmias in the late myocardial infarction period: 17. Correlation of activation patterns of sinus and reentrant ventricular tachycardia.

The relationship between myocardial sites with late activation during sinus rhythm and sites critical for the initiation and sustentation of reentrant ventricular tachycardia was systematically examined in the 4-day-old postinfarction canine heart. The critical sites for prevention of the initiation of reentry and for termination of sustained figure-of-8 reentrant tachycardia by cryothermal techniques were correlated with the last 20 msec isochrone during sinus rhythm. In 12 experiments, 20 critical sites were examined. The mean distance between sites critical for reentry and the latest isochrone during sinus rhythm was 26.7 +/- 13.3 mm. Only five sites (25%) were within a 12 mm distance, which corresponded to the diameter of the cryoprobe. Nine sites (45%) were within a 24 mm distance (twice the diameter of the cryoprobe), while 11 sites (55%) were separated by more than 24 mm. In three experiments the sites of latest activation during sinus rhythm represented areas showing Wenckebach period or 2:1 conduction block. These sites became dissociated and did not participate in the reentrant excitation induced by premature stimulation. Poor correlation was explained by the fact that sites critical for reentry were intimately related to the location and extent of the arcs of functional conduction block while sites of delayed activation during sinus rhythm were not.

Animals↗
PubMed1990

Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: a potential new approach to the management of ischemia-induced malignant ventricular arrhythmias.

The increase in extracellular potassium [K+]o levels during the early phase of myocardial ischemia may result in part from activation of adenosine triphosphate-sensitive K+ channels. Glyburide, a second-generation hypoglycemic sulfonylurea, is a potent blocker of these channels. We studied the effects of glyburide on [K+]o and on intramyocardial conduction delay during a 10-minute occlusion of the left anterior descending artery in the dog. K(+)-sensitive electrodes and bipolar plunge electrodes were introduced to record, respectively, [K+]o and local electrograms from close sites in midmyocardial regions in normal, border, and ischemic zones. Recordings were obtained before (control ischemia [CI]) and 20 minutes after intravenous administration of 0.15 mg/kg of glyburide (glyburide plus ischemia [G + I]). During G + I the extent of the increase in [K+]o was less compared to that during CI, and the difference was statistically significant during the first 7 minutes of ischemia in the ischemic zone and during the first 4 minutes of ischemia in the border zone. On the other hand, the degree of local intramyocardial conduction delay was significantly reduced during G + I compared to CI during the entire 10 minutes of ischemia in both the ischemic and border zones. In summary, our results have shown that glyburide significantly reduced the rise of [K+]o and intramyocardial delay during the early phase of acute ischemia and could thus attenuate the electrophysiologic consequences of ischemia that underlie the initial phase of malignant tachyarrhythmias. Although the effects of glyburide may result in part from a direct action of the drug on cardiac adenosine triphosphate-sensitive K+ channels, other metabolic antiischemic effects cannot be ruled out.

Animals↗
PubMed1990

Electrophysiological effects of a chemical defibrillatory agent, dibenzepin.

STUDY OBJECTIVE: The aim was to study the cellular cardiac electrophysiological effects of the antifibrillatory drug, dibenzepin. DESIGN: Standard microelectrode techniques were used to measure the effects of dibenzepin (3 microM, 9 microM) on conduction time, Vmax and input resistance in canine papillary muscles, in vitro, at three paced cycle lengths (1000, 400, 200 ms). Results were compared when adrenaline (0.5-5 microM) or propranolol (0.2 microM) were present. EXPERIMENTAL MATERIAL: Papillary muscles (n = 25) from hearts of adult mongrel dogs, weight 13-18 kg, were used. MEASUREMENTS AND MAIN RESULTS: Dibenzepin, at 3 microM, caused significant reduction of Vmax at cycle lengths less than or equal to 400 ms. Paradoxically, the conduction time decreased at all three cycle lengths when measured along the longitudinal axis of the fibre between two microelectrodes spaced 2 mm apart. Superfusion of dibenzepin (3 microM) and propranolol (0.2 microM) significantly reduced Vmax and lengthened conduction time at all cycle lengths. Dibenzepin reduced input resistance from 1.45 to 0.76 M omega, thereby suggesting that improved coupling may occur between cells to account for the shortening of conduction time. Propranolol blocked these results. CONCLUSION: The defibrillatory action of dibenzepin may be related to a decreased intercellular resistance caused by increased catecholamine availability during fibrillation. This would result in improved conduction and, thereby, a decrease of the critical number of asynchronous re-entrant circuits necessary to maintain fibrillation.

Action Potentials↗
PubMed1990

A logical state model of reentrant ventricular activation.

The ventricular surface of the heart was modeled as two-dimensional, 4096 element, network of cells connected logically to each other. An ischemic area was represented by a central core of prolonged refractoriness, distributed into eccentrically-layered elliptical contours such that refractoriness declined along varying gradients to the surrounding normal area. Propagation of cardiac action potentials was stimulated by five sequential states ranging from activation to inactivation. Reentrant activation was induced by premature stimulation of the network and resembled a "figure 8" type reentry seen experimentally. Activation patterns of reentry appeared as two propagation wavefronts which traveled around the ends of a continuous line of functional conduction block, merged into a single wavefront, then conducted slowly along a retrograde path to reactivate a region proximal to the block. Reentry could be prevented by modifying the distribution of recovery of excitability through stimulation at two strategically located sites during basic rhythm. Prevention occurred when the second site was situated in an area of prolonged refractoriness, just distal to the line of block. These simulations indicate that reentrant activation is characterized by the formation of long lines of conduction block which occur along a border of steeply graded refractoriness, and retrograde slow conduction which occurs along a more shallow refractory gradient. The occurrence of reentry is dependent on: 1) the coupling interval of the premature stimulus, 2) the location of the stimulus relative to the maximum refractory gradient, and 3) the activation sequence of the basic paced beats. Thus, this paper presents an efficient logical state model of cardiac activation which simulates experimentally observed activation patterns of reentry and its prevention.

Action Potentials↗
PubMed1990

Electrophysiological basis of ventricular late potentials.

The presence of late potentials on the body surface recording was correlated with ventricular activation maps of reentrant circuits in the postinfarction canine model of reentrant excitation. Late potentials were found to correlate with delayed myocardial activation. However, during a reentrant rhythm complete diastolic activity on the body surface could not be detected if the mass of electrically active cells was too small and/or if very slow conduction in part of the reentrant circuit generated low amplitude extracellular potentials. Myocardial zones responsible for late potentials during a basic rhythm (e.g., sinus rhythm) may not necessarily be part of the critical zone of slow conduction during reentrant activation. Dynamic changes in late potentials are not amenable to temporal signal averaging techniques but could be detected by a high resolution beat-to-beat recording. A thorough understanding of the electrophysiological limitations of late potentials in the signal-averaged ECG could result in better utilization of the technique in clinical practice as well as in the development of new approaches for the detection of the arrhythmogenic substrate.

Action Potentials↗
PubMed1990

The signal averaged electrocardiogram and programmed stimulation in patients with complex ventricular arrhythmias.

The signal averaged electrocardiogram (SA-ECG), programmed electrical stimulation (PES), and left ventricular ejection fraction (EF) studies were utilized for risk stratification and management of patients with complex ventricular arrhythmias and nonsustained ventricular tachycardia (VT). The study population included 90 patients (63 with coronary artery disease and 27 with dilated cardiomyopathy). Sustained monomorphic VT was induced in 22 cases (24%), ventricular fibrillation (VF) in 10 (11%), and no sustained VT/VF in 58 (64%). An abnormal SA-ECG was recorded in 23 patients (26%) and was more common in patients with than in those without induced sustained VT (68% vs 12%, P less than 0.0001). None of 33 patients with normal SA-ECG and EF greater than or equal to 40% had induced VT. Patients were followed-up for 2.5 +/- 0.8 years off antiarrhythmic therapy, unless they had induced sustained VT. The 3-year sudden death rate was 19% in the group with induced sustained VT, 0 in that with induced VF, and 9% in that without induced VT/VF (P = NS). The 3-year total cardiac mortality was higher in patients with than in those without EF less than 40% (27% vs 7%, P less than 0.05). It is concluded that patients with organic heart disease and spontaneous nonsustained VT may not need PES or antiarrhythmic therapy if SA-ECG is normal and EF is greater than or equal to 40%, since their risk of induced VT and sudden death is low. On the other hand, patients with abnormal SA-ECG and/or EF less than 40% may require PES, since their risk for induced VT is high. Antiarrhythmic therapy may also be considered in these patients.

Action Potentials↗
PubMed1990

Effects of caffeine and ryanodine on delayed afterdepolarizations and sustained rhythmic activity in 1-day-old myocardial infarction in the dog.

Caffeine and ryanodine are known to modulate oscillatory release of Ca2+ from the sarcoplasmic reticulum. The effects of caffeine and ryanodine on delayed afterdepolarizations (DADs) and sustained rhythmic activity in subendocardial Purkinje fibers surviving 1-day-old myocardial infarction in the dog were studied with standard microelectrode techniques. In preparations that showed sustained rhythmic activity, a high concentration of caffeine (10 mM) and ryanodine (10(-7) and 10(-6) M) slowed and terminated the sustained rhythmic activity and markedly suppressed DADs. An increase in the temperature of the tissue bath from 37 degrees to 39 degrees C did not change these results. In quiescent normal and infarcted preparations, a low concentration of caffeine (0.5 mM) differentially induced DADs in ischemic but not in normal Purkinje fibers, increased the amplitude of existing DADs, and brought subthreshold DADs to threshold potential that caused triggered activity. Our results are consistent with the hypothesis that triggered activity arising from DADs characterizes the sustained rhythmic activity in endocardial preparations 1 day after infarction and indicate an important role for the sarcoplasmic reticulum in the genesis of DADs and triggered activity in this model.

Alkaloids↗
PubMed1990

Ventricular arrhythmias in the subacute myocardial infarction period. High-resolution activation and refractory patterns of reentrant rhythms.

Patterns of activation, functional conduction block, and effective refractory periods during reentrant activation were investigated in a 4-day postinfarction canine model using a 64-channel high-resolution (1 mm) bipolar electrode array. Lower resolution (3-10 mm) isochronal activation maps of the entire epicardial surface were constructed from 126 sites during the initiation and sustenance of reentry and showed reentrant wave fronts that circulated around arcs of functional conduction block. During initiation of reentry by premature stimulation, high-density recordings from these same regions showed that conduction block occurred abruptly, within 1 mm, and without prior decrement of the impulse. Electrograms recorded in proximity to the arc of block were comprised of two deflections: a local activation potential and an electrotonic potential reflecting activation 1 mm away; the reverse order of activation and electrotonus was observed on the opposite side of the arc of block. The occurrence of functional conduction block during premature stimulation in this model was correlated with abrupt increases in effective refractory periods of 10-120 msec (27 +/- 24 msec; mean +/- SD) within 1 mm or less. Neither the abrupt change of refractoriness nor functional conduction block appeared to depend on differences in excitability, the geometrical characteristics of the surviving epicardial layer, or the orientation of the myocardial fibers. During sustained reentrant activation, high-density recordings along the arcs of block showed split electrograms comprised of local activation and electrotonus, which were identical in morphology to those recorded during the initiation of reentry. The interval between the deflections was shorter at the ends of the arc and increased to a maximum value at the center of the arc. The activation potentials corresponded in time with activation of large isochronal regions on either side of the arc of block. There was evidence that at least part of the arc of block during sustained reentry represented thin discrete zones of constant block due to electrotonic influences of impulse penetration from both sides of the arc. Our results strongly suggest that continuous arcs of functional conduction block are a necessary prerequisite for both the initiation and the sustenance of reentrant activation in subacute canine myocardial infarction. Functional conduction block during the initiation of reentry was due to abrupt changes in refractoriness, within a distance of 1 mm or less.

Animals↗
PubMed1990

Circus movement atrial flutter in the canine sterile pericarditis model. Activation patterns during initiation, termination, and sustained reentry in vivo.

The mechanisms of single-loop reentry in a syncytium without anatomically predetermined pathways have not been shown. Using a "jacket electrode" with 111 bipolar electrodes in a nylon matrix, we mapped in situ the atrial epicardial surface during atrial flutter in dogs with sterile pericarditis. Of 21 episodes of reentrant atrial flutter, only four showed double-loop ("figure-eight") reentry, whereas in 17 episodes a single loop was present. During initiation of single-loop reentry, an arc of functional block extended to the atrioventricular (AV) ring. This forced activation to proceed as a single wave around the free end of the arc, before breaking through the arc close to the AV ring. Activation continued as one loop around an arc close to the AV ring (in eight episodes) or around a combined functional and anatomic obstacle (in nine episodes) when the arc joined an atrial vessel. A zone of slow conduction was consistently bordered by the arc of block and the AV ring or by the anatomic obstacle and the AV ring. Spontaneous termination occurred when conduction failed in this area and the arc rejoined the AV ring. High-density recordings (2 mm) along the arc of block showed double potentials separated by an isoelectric interval, interpreted as local activation and electrotonus due to activation on the opposite side of the arc. Histologically, a diffuse inflammatory reaction involved 50-80% of the atrial wall. A transitional layer of myocardial bundles with preserved cross striation, but separated by edema and inflammatory cells, was enclosed between an epicardial layer of fragmented myocytes and an endocardial layer of grossly intact myocardium. There were no distinctive features at sites of functional conduction block or slowed conduction. In conclusion, single-loop reentry is the common pattern during atrial flutter in this model. Its induction depends on an interaction of the AV ring, a functional arc of block, and a zone of slow conduction. The location of the inferior vena cava predisposes the lower right atrium to this type of reentry.

Animals↗
PubMed1990

Risk stratification and management of patients with organic heart disease and nonsustained ventricular tachycardia: role of programmed stimulation, left ventricular ejection fraction, and the signal-averaged electrocardiogram.

PURPOSE: Programmed stimulation, left ventricular ejection fraction, and signal-averaged electrocardiography were performed in patients with organic heart disease and spontaneous nonsustained ventricular tachycardia (VT) to determine the role of these techniques in risk stratification and management. PATIENTS AND METHODS: The study consisted of 90 patients: 63 had coronary artery disease and 27 had idiopathic dilated cardiomyopathy. Radionuclide ventriculography, signal-averaged electrocardiography, and programmed electrical stimulation were performed in all patients within 48 hours of index ambulatory electrocardiography. RESULTS: Fifty-three patients (59%) had an ejection fraction less than 40%. Programmed stimulation induced sustained monomorphic VT in 22 patients (24%), ventricular fibrillation (VF) in 10 patients (11%), and no sustained VT/VF in 58 patients (64%). The signal-averaged electrocardiogram (ECG) showed late potentials in 23 patients (26%). Sustained monomorphic VT could be induced in 65% of patients with late potentials and in 10% of those without late potentials. There was no case of inducible sustained monomorphic VT in 33 patients with no late potentials and an ejection fraction of 40% or greater. All patients with induced sustained monomorphic VT received antiarrhythmic therapy guided by the results of programmed stimulation. All 58 patients with no induced sustained ventricular tachyarrhythmias and eight patients with induced VF were discharged without receiving antiarrhythmic drugs. During a follow-up of 30 +/- 10 months, the three-year sudden death rate was 19% in patients with induced sustained VT, 0% in those with induced VF, and 9% in those with no induced sustained VT/VF. The three-year sudden death rate was the same (7%) in patients with no induced sustained VT/VF, both in those with an ejection fraction of 40% or greater or less than 40%. On the other hand, the three-year total cardiac mortality was significantly higher (27%) in those patients with ejection fractions less than 40% compared to those with ejection fractions of 40% or greater (7%). CONCLUSION: It is concluded that the signal-averaged ECG, ejection fraction, and programmed stimulation could be used for the risk stratification and management of patients with organic heart disease and nonsustained VT as follows: (1) Patients with no late potentials and with an ejection fraction of 40% or greater do not require invasive evaluation or antiarrhythmic therapy, since the incidences of induced VT and sudden death are very low. (2) Patients with late potentials as well as patients without late potentials but with an ejection fraction of less than 40% may be advised to undergo electrophysiologic evaluation.(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗
PubMed1989

Role of bandpass filters in optimizing the value of the signal-averaged electrocardiogram as a predictor of the results of programmed stimulation.

Normal values for the signal-averaged electrocardiogram (SAECG) at 11 different high-pass filter settings were obtained from 100 normal subjects (group I). The filtered QRS duration and the duration of low amplitude signals less than 40 microV, but not the root mean square voltage of the last 40 ms (RMS40), showed normal distribution. A normal distribution for RMS40 could be obtained by transforming each value to its natural logarithm. The normal values were used in a systematic approach to optimize the accuracy of the SAECG to predict the results of programmed stimulation in 80 patients with spontaneous nonsustained ventricular tachycardia (VT). Fifty-two patients with no inducible VT (group II) and 28 patients with inducible sustained monomorphic VT (group III) were investigated. The 3 SAECG parameters at each high-pass filter in groups II and III were categorized as normal or abnormal and were evaluated singly or in combinations of 2 or 3. There was no combination that provided a sensitivity greater than 82% that could also be obtained by single determinations of low amplitude signals less than 40 microV at 25 to 40 Hz or RMS40 at 40 Hz. On the other hand, there were 267 different combinations that provided a maximal specificity of 98%. The best total predictive accuracy of a single parameter was 85%, provided by RMS40 at 40 or 60 Hz. The total predictive accuracy could be improved to 89% by 1 of 32 different combinations. The top combinations were mostly in triplets and included SAECG parameters recorded at different high-pass filter settings. The only 2 paired combinations with the best total predictive accuracy were RMS40 at 20 or 25 Hz paired with RMS40 at 40 Hz. Frequencies at both ends of the analyzed high-pass filter settings (less than 20 Hz and greater than 60 Hz) were not represented in the top predictive combinations. The SAECG parameters analyzed at 40 Hz were most frequently represented in the top predictive combinations, suggesting that the SAECG may have the best predictive accuracy at this filter setting. In summary, the combination of SAECG parameters analyzed at different filter settings can enhance the accuracy of the technique as a screening test for the results of programmed stimulation in patients with spontaneous nonsustained VT.

Adult↗
PubMed1989

Correlation between the signal-averaged electrocardiogram from Holter tapes and from real-time recordings.

Signal-averaged electrocardiograms obtained from 3-channel Holter recordings were compared, using the same skin electrodes, with signal-averaged real-time recordings in 32 subjects. The numeric late potential parameters and morphologic appearances correlated closely between the 2 methods. The restricted high frequency response of Holter systems appears not to militate against clinically useful late potential analysis from Holter tape. This study suggests that diagnostic accuracy using real-time 25 to 250-Hz criteria is acceptable for clinical use until criteria derived specifically for Holter applications become available. Holter analysis may confer significant benefits resulting from an ability to perform late potential analysis on the same tape used for conventional arrhythmia analysis, and would allow future studies of possible dynamic changes of late potentials in relation to transient ischemia and spontaneous ventricular tachyarrhythmias.

Arrhythmias, Cardiac↗
PubMed1989

Stretch-activated ion channels in cultured mesangial cells.

Membrane stretch, delivered by negative pressures in cell-attached patch pipettes, activated single-channel ionic currents in cultured mesangial cells. Channel opening probabilities were directly related to degree of suction, with threshold for activation being 5-10 mm Hg. The stretch-activated channels were permeable to Na+, K+, as well as Cl-, having conductances averaging 62 +/- 17 pS. These channels may represent a cellular mechano-reflex in mesangial cells.

Animals↗
PubMed1989

Prognostic significance of the signal-averaged ECG depends on the time of recording in the postinfarction period.

Serial recordings of the signal-averaged ECG and the 24-hour ambulatory ECG were obtained from 156 patients with acute myocardial infarction up to 5 days (phase 1), 6 to 30 days (phase 2), and 31 to 60 days (phase 3) after the infarction. Left ventricular ejection fraction by radionuclide ventriculography was also determined in phase 2. The signal-averaged ECG was abnormal during one or more of the three phases in 51 patients (31%). In 35 of these patients (69%) the recording changed category between normal and abnormal with the highest prevalence of abnormal recording occurring during phase 2. Eight patients had ventricular tachycardia/ventricular fibrillation in the first 48 hours after myocardial infarction. The signal-averaged ECG was abnormal in only one of these patients. Twelve patients had late arrhythmic events during the first year of follow-up (four sudden deaths and eight instances of documented ventricular tachycardia or ventricular fibrillation). Nine of the 12 patients had an abnormal signal-averaged ECG in phase 2 and four of these nine had a normal recording in phase 1. Five patients had a transient abnormal signal-averaged ECG in phase 1, whereas six patients had an abnormal recording only in phase 3. None of these 11 patients had an arrhythmic event. Stepwise logistic regression showed that an abnormal signal-averaged ECG in phase 2 has the most significant relation to late arrhythmic events. Both an abnormal signal-averaged ECG and a left ventricular ejection fraction less than 40%, but not complex ventricular arrhythmias, were independent significant risk factors for late arrhythmic events.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗