Premise of Sleep and Heart Attack

Sleep is modified by psychosocial settings stored up during routine daily activity. Just as that short-term memory plays a role in modify-ing sleep behavior, long term stress also instigates such disbalance. The degree of disbalance would mount assertively if the source of in-trigue also persists during sleep. Similarly an extreme degree of auto-nomic disbalance is eventuated, when somatic afferents fire at a greater frequency due to frictional electricity produced in the bed when particularly synthetic clothing and synthetic bed lenin is used. It is also anticipated that these influences would also instigate coronary vasospasm, nocturnal angina besides instigating cardiac irregulari-ties of all grades. These influences are likely to disrupt the normal sleep; dream and even the sensual behavior other than sleep apnea related problems due to failure in rhythmogenesis.

Sleep – Related Respiratory Disorders:

One of the remarkable developments in medicine has been the recog-nition of a diverse group of clinical problems that originate in breath-ing disturbances during sleep. These disorders have been classified as sleep apnea divided into central (failure of rhythmogenesis) or ob-structive (upper airway occlusion) types; hypopnea; respiratory dis-ease with deterioration during sleep; and nocturnal yearning and aspi-rations. Apnea during sleep is defined as a cessation of airflow at the nose and mouth for at least 10 Seconds.

Although such episodes are seen in normal persons, as they grow older, these episodes are usually infrequent (less than five episodes/h of sleep). By contrast, patient with sleep apnea that is clinically im-portant has hundreds of episodes that permeate sleep, altering its structure, with potential life-threatening sequelae. The special influ-ence of sleep on the respiratory center causes two basic patterns of apnea.

This transition is probably influenced by age and body weight. The repetitive apneic events cause profound oxygen desaturation of he-moglobin and fragmentation of sleep with the characteristic-presenting symptom of excessive somnolence during the day. The pa-tients are usually middle-aged men or postmenopausal women who are overweight and have experienced a recent increase in body girth. They are often hypertensive and have a history of loud snoring. Other related clinical manifestations include headaches in the morning, learning disabilities (mostly in children), personality and intellectual changes, sensual impotence, abnormal motor activity during sleep, and nocturnal insomnia. Cardiac arrhythmias and angina may be pre-senting symptoms at night and sudden death may occur in these pa-tients. Pulmonary hypertension and erythrocytosis may occur, espe-cially in the presence of an underlying lung disease. Failure of the left ventricle may be seen with severe obstruction due to increased cardiac afterload, which may occur during upper airway obstruction. Alveolar hypoventilation during wakefulness, defined as an elevation in arterial carbon dioxide pressure (PaCO2), is uncommon in patients with ob-structive sleep apnea. The classic pickwickian patient with the obesity hypoventilation syndrome has alveolar hypoventilation during wake-fulness. Many of these patients have obstructive sleep apnea are not pickwickian.

Central sleep apnea syndromes are less common and are found in less than 5% of patients. Neurologic disorders such as poliomyelitis, en-cephalitis, brain-stem infarction or neoplasm, cordotomy, and spinal surgery may affect the respiratory center and cause periodic cessation of breathing during sleep. Primary hypoventilation syndromes also occur.

Disturbed Sleep with sleep apnea due to failure in rhythmogenesis, also called Alien Abduction Behavior often experienced when the subject is half asleep half awake, can perceive but can not speak or move. Other related problems include headaches in the morning, eru-dition of lethargy and personality changes. Intellectual changes, sen-sual impotence abnormal motor activity during sleep, cardiac ar-rhythmias, angina may be a presenting symptoms at night and even sudden sleep death may occur in many patients.

We have observed that: Sleep apnea with restless leg syn-drome due to failure in rhythmogenesis without any underly-ing systemic or cardiovascular disease, the incidence was 0.24% wearing cotton and it was 4.67% wearing synthetic garments.

The REM (rapid eye movement) state of sleep is the time when the throat is most likely to relax and close up. Blood oxygen level plum-mets and the diaphragm is racked by contractions to 49%, and the heart is slowed to 40 beats a minute. Stress like this can damage the heart and makes apnea a life–threatening conditions.

If apnea is ascertained early, dropping weight, restraining alcohol and eradicating smoking is eventually satisfactory. Swathing over to cot-ton Pajama and lenin instead of synthetics have helped 75% of our patients to discomfit sleep affiliated nuts and doubts when there was no distinct explanation discernible. Once the medical community be-comes accurately enlightened about this state of being, apnea’s gull and dupes will have a preferred possibility of getting a good night’s sleep.

People say obscure and lax things like ‘I feel, sickly, frail, feeble, tired and fatigued’. Most people require seven to nine hours of shut-eye a night, but many of us get less. As truck drivers have found, that can be dangerous, leading to microsleeps – brief periods, lasting one to ten seconds, when you are snoozing even though your eyes are open.

Sleep well:

When you have lost enthusiasm, delight and interest make up for it by going to bed earlier the next night. If you can not, you might sleep longer on weekends to catch up. Another way: During break, take a 20- to 40-minute snooze and siesta.

Have trouble sleeping?

It’s natural to have sleepless nights when you are stressed-out or ill. If those are not the reasons, avoid caffeine within six hours of bedtime. Go to bed only when you are tired; if you are still awake after 20 minutes or so, get up and read or watch some interesting movie on TV until you feel like swinging and drooping off. If insomnia persists, or if daytime drowsiness interferes with work, see a doctor. But be con-vinced that in most of the situations getting rid of synthetic garments worn next to the skin and used for bed lenin besides synthetic carpets and curtains will help you return to a sound natural sleep.

Enigma of Sleep Death

Various names have been given to sudden unexplained sleep death, the phenomenon described in piles of literature in different societies “Bangungut” in Tagalog (literally, to rise and moan), “Pok-Kuri” (sudden death) described by Japanese workers, and “Non-Lai-Tai” (literally, sleep death) described by Laotians.

Classic risk factors such as hypercholesterolemia, hypertension, and smoking identify subjects predisposed to coronary heart disease (CHD) but do not help segregate those especially predisposed to sud-den death. A review of current literature, with other interesting obser-vations, will probably highlight the recent increase in the incidence of sleep death.
To speak frankly in modern scientific orientation and conviction, the contemporary epidemic of premature sudden death, along with its un-derlying disease process, is due fundamentally to the evolution of the twentieth-century lifestyle, particularly during the past fifty years.

So-cioeconomic development has led to the replacement of tuberculosis by coronary disease as the mass disease of the adult population. That is, coronary epidemic, like the earlier TB epidemic, is essentially so-cial in origin. It is due particularly to the evolution of nutritional hab-its, sedentary living, smoking, and by personality behavior pattern Sudden coronary death accounts for almost fifty percent of all deaths. This, of course, is nothing new; the risk of sudden death, sizeable as it is for middle-aged men free of evidence of CHD, is far greater for those with clear-cut evidence of coronary disease. With these facts in mind, it seems appropriate to define sudden death as the event in the greater majority of the young adult and middle-aged population which is free of evidence of coronary disease and generally well clinically. Sudden death, when it occurs free of evidence of any organ system disease, is called sudden unexplained death.

In most healthy individuals, the cardiac rhythm originates from the primary pacemaker, the sinus node, and is termed sinus rhythm. Many patients with cardiac disease may also have sinus rhythm. Similarly, the occurrence of an ectopic rhythm, particularly Ventricular Prema-ture Beats, does not always indicate cardiac abnormality and may oc-cur in individuals free of evidence of any organ-system disease. Be-sides pathological substrate of sudden cardiac death (Table 1), cardiac arrhythmias, or VBPs, may occur due to many factors, e.g., age, car-dioinhibitory and cardioacceleratory forces, chemical mediators, smoking, tea, coffee, alcohol, posture, position, exercise, and emo-tional disbalance.

Behavioral attitude is obligated to poised working of the autonomic nervous system. We may achieve autonomic peace by various tech-niques, including psychological and cardiological counseling, by us-ing B-adrenergic blockers and minor tranquilizers, or by transcenden-tal meditation, i.e., yoga, Sufism, and even physical exercises. We may achieve genuine autonomy of the autonomic nervous system, but if we fail to restore it permanently, we may still be confronted by be-havioral problems, which are accompanied by increased sympathetic drive and increased quantity of catecholamine released per unit of time.

A challenging question has been to identify the trigger for terminal arrhythmia, which results in nearly instantaneous fatality.

Further research will focus attention on the following lines:

1. Underlying arrhythmia accounting for the terminal mechanism is runs of multifocal ventricular ectopics, or ventricular tachycardia degenerating into VF.

2. Electrophysiologic lesion in the myocardium that permits reen-trant disorganized propagation of depolarization wave front is the basis of VF and coronary heart disease is a usual cause of electri-cal instability. The electrophysiologic abnormality, once it emerges, is independent of the anatomic substance and affects the heart rhythm in a way that culminates in lethal arrhythmias.

3. Certain types of VPBs reflect the presence of electrical instability, and their occurrence in patient with IHD predisposes them to re-petitive ventricular activity which may trigger VF.

4. In the electrically unstable heart, momentary changes in myocar-dial excitable properties, designated as transient risk factors, can provoke VF. These risk factors include neural traffic to the heart initiated by psychological inputs.

At times, individual clinical experiences have provided profound pathophysiologic insight. Wallen and associates have described a fourteen-year-old girl who first lost consciousness on being awakened one night by a thunderclap. Thereafter she had repeated syncopal at-tacks caused by self-terminating ventricular fibrillation. Waking her with a variety of auditory stimuli provoked these attacks. The electro-cardiographic sequence was consistent and began with sinus tachy-cardia, followed by prolongation of QT interval, inversion of T wave, and emergence of VPBs, culminating in VF.

In my clinical experience I had a chance finding of association of ven-tricular arrhythmias with the blend of garments worn next to the skin in an eleven-year-old boy. This boy was initially evaluated at the Sec-tion of Cardiovascular Diseases, School of Medicine, and University of California Davis, United States, for the cardiac irregularity (ven-tricular bigeminal rhythm) that was discovered during a routine physical examination at his school.

The detailed case study is reproduced.

Case History

An eleven-year-old boy was first noted to have an arrhythmia approximately eight to ten months ago while exercising at school. The arrhythmia was discovered quite by accident on an examination because he had complained of some exercise intoler-ance. The only significant past history from a cardiovascular standpoint is that he has had two episodes of acrocyanosis, both of which occurred while swimming. There was no history of syncope, chest pain, or dizziness associated with the acro-cyanosis or occurring as an isolated problem.
Of other significant history is the fact that in 1977 he has his left kidney removed because it was nonfunctioning, probably secondary to severe obstruction.

His previous workout, from the arrhythmia standpoint, in Pakistan, has included echocardiography and exercise testing, both of which were said to have been nor-mal. He does not have symptoms every day, but his exercise has been limited on the recommendation of his physician. Multiple medications have been tried singly and in combination to suppress his arrhythmia, and these have been uniformly unsuc-cessful. Medications have included propranolol, procainamide, and Norpace.

On physical examination today, heart rate is 96 and irregular, respiration 16 and non-labored, and blood pressure 124/66. His height is 146 cm and his weight is 43.7 kg. In general, this is an alert, acyanotic, mildly overweight boy who is cooperative and in no distress. Examination of the neck reveals no venous distention and no carotid bruits are audible. Auscultation of the chest is clear. Examination of the heart reveals a regularly irregular rhythm. The pericardium is quiet. The first heart sound and second heart sounds are normal.

A grade I-II/VI systolic ejection murmur is heard at the mid-left sternal border and diastole is clear. No hepatosplenomegaly is noted and pulses are full in all extremi-ties. There appears to be a bigeminal rhythm as detected by auscultation and by pal-pation of the pulses during which a strong pulse is followed by a weaker pulse.

Chest x-ray taken today shows normal heart size and configuration with normal pulmonary blood flow. An electrocardiogram shows mostly a ventricular bigeminal rhythm. The sinus beats demonstrate a normal axis with no evidence of atria en-largement or ventricular hypertrophy. The ventricular extrasystoles are uniform in morphology with a constant coupling interval to the sinus beats. The Q-T interval is normal and no R-on-T phenomena are noted.

M-mode and 2-D echocardiography were performed and both appear to be normal. It must be pointed out, however, that with this patient having a bigeminal rhythm, all of his beats are either extrasystolic or postextrasystolic. Someone would not nec-essarily expect normal end diastolic volume to any of his ventricular contractions. There is, however, normal anatomy and what appears to be normal function with no evidence of masses on the echo.

An exercise treadmill was performed. He was able to exercise for just over seven and one-half minute before stopping the test because of fatigue. The ventricular bigeminy rapidly changed to basically sinus rhythm with rare ventricular extrasysto-les simply by having him stand up. At one minute of exercise, the arrhythmia was entirely suppressed and the rhythm was entirely sinus with a rate of approximately 115 beats/min. throughout, the exercise treadmill test, no further arrhythmias were noted and no significant ST segment changes were evident. Following the exercise treadmill test, at one minute post-exercise ventricular extrasystoles were again noted occasionally and the bigeminal rhythm was noted by four minutes following the exercise when the heart rate had diminished to approximately 103 beats/min. Blood pressure was normal throughout the exercise treadmill test as expected.

His heart had a somewhat unusual, but no unheard of, problem in pediatrics known as frequent ventricular extrasystoles in what appears to be an otherwise normal heart (Figure 1). Little is written about this in the literature; however, what is available suggests that the following findings are helpful in determining whether this ar-rhythmia is serious or benign:

No evidence of heart disease

1. Uniform morphology to the ventricular extrasystoles
2. Constant coupling interval of the ventricular extrasystoles
3. Normal Q-T interval
4. Absence of R-on-T phenomenon
5. Complete suppression of the arrhythmia with exercise

Discussion

Occurrence of ventricular arrhythmias originating from the right ven-tricle but without severe underlying myocardial disease is now well recognized and has been termed arrhythmogenic right ventricular dysplasia. At present there is insufficient long-term prognostic data in this group of patients. But frequent VPBs (Ventricular bigeminal rhythm), as in this case; indicate electrical instability of the myocar-dium. It is now well established that non-uniform cardiac recovery properties enhance vulnerability to and favor persistent fibrillation.

It had been my routine to record EKG trace with cotton blends, be-cause previously the wave forms abnormalities were observed by me in-patients wearing synthetic clothing. These wave form abnormali-ties were often confused for ischemic changes, and quite frequently ischemic changes were masked by the disturbed surface body poten-tial. After giving cotton clothing to this patient, I got busy with my routine OPD and did not ask the nurse to record EKG before one hour. When after one hour, if switching over to cotton clothing EKG was recorded? It occasionally showed PVCs. I waited for another one hour and after two hours of switching over to cotton clothing EKG was recorded, it occasionally showed PVCs. I waited for another hour, and after two hours of switching over to cotton clothing there were no VPBs. This procedure was repeated many times, and it showed quite a significant influence of type of garment (Table1). It instigated us to start work on this subject, which had not been re-ported or documented earlier.

Table1

Frequency of PVCs at various intervals
After wearing different blends of garments
Type of garments Intervals (h) Frequency of PVCs
Own 1st 3600
Cotton 2nd 600
Synthetic 3rd 3000
Synthetic 4th 3600
Cotton 5th 600
Cotton 6th 0

(PVCs were given in round figures if these were more than ³ 50 these were added to 100 and if less than 50 than 0)

The influence of synthetic garments on the body surface to the pro-duction of PVCs was an interesting observation. As we have dis-cussed, the increasing incidence of PVCs presents a real therapeutic challenge. We have shown the relationship of PVCs to the quality of garments worn next to the skin. Data analyzed in this report was ob-tained from our initial reports published during the period from 1982 to 1989. These studies were designed to assess the influence of the type of garments worn next to the skin on Ventricular Premature Beats both in hospitalized and civilian non-institutionalized popula-tion based on clinical history and physical examination of 4,000 rep-resentative individuals selected by complex probability sampling pro-cedure

Two thousand subjects were wearing synthetic clothing at the time of examination, and the other 2,000 were wearing cotton clothing.