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SUBMITTED TO DELHIUNIVERSITY
NEW DELHI
FOR DEGREE OF
MD (GENERAL MEDICINE)
2015- 2018
TOPIC
“STUDY OF SLEEP APNOEA IN PATIENTS WITH STABLE HEART FAILURE”
BY
MAJ (Dr) VISHAL JHA
RESIDENT
DEPARTMENT OF MEDICINE
ARMY HOSPITAL(RESEARCH AND REFERRAL)
UNDER GUIDANCE OF
BRIG (Dr) NAVEEN AGGARWAL
HEAD OF THE DEPARTMENT
DEPARTMENT OF CARDIOLOGY
ARMY HOSPITAL(RESEARCH AND REFERRAL)
DELHI CANTT- 110010
To
The Dean
University of Delhi
Dear Sir,
I have registered my name with your esteemed University in June 2015 for award of M.D.(General Medicine)
under the guidance of BRIG(Dr) NaveenAggarwal. The suggested topic of thesis is as under:
It is requested that necessary approval may be given for the above, please.
Thanking You,
Yours sincerely,
We have jointly examined all the ethical issues related to thesis titled “STUDY OF SLEEP APNOEA
IN PATIENTS WITH STABLE HEART FAILURE” being done by
DrVISHAL JHA and have given the following recommendations.
Dy Commandant
Chairman
OIC Pathology
COUNTERSIGNATURE
--------------------------------------------------
1 Title Page 1
2 Certificate by guide 2
3 Introduction 3-4
6 Performa 14-15
7 Questionnaire 16
8 References 17-18
1
SESSION : 2015-2018
CERTIFICATE
I certify that facilities for work on this subject of thesis, “STUDY OF SLEEP APNOEA
IN PATIENTS WITH STABLE HEART FAILURE”exist in this department and will be
provided to the candidate. I shall see that the data being included in the thesis is
genuine and the work is done by him.
Title:
Introduction:
One in five adults suffers from at least mild sleep apnea, and it afflicts more men than women. The
most common type is obstructive sleep apnea in which fat in the upper chest and neck contributes to
blocking the flow of air. (Another type, called central sleep apnea, is far less prevalent).
Obstructive sleep apnea (OSA) is associated with obesity, which is also a major risk factor for heart
disease and stroke. Besides obesity contributing to sleep apnea, sleep deprivation caused by sleep
apnea can, in an ongoing unhealthy cycle, lead to further obesity. In OSA the upper airway closes off
because the muscles that hold it open lose tone - the more weight, the more loss of tone and the more
severe the sleep apnea. Each time the airway closes; there is a pause in breathing.
Another type of sleep apnea, called central sleep apnea (CSA), is far less prevalent.) In CSA the brain
doesn’t send regular signals to the diaphragm to contract and expand. There is limited snoring with
CSA, and it has been associated with brain stem stroke because the brain stem is where the impulse
to breathe comes from. In a sleep study, doctors count pauses in breathing to determine whether the
patient has mild sleep apnea, characterized by five to 15 episodes per hour; moderate sleep apnea,
defined by 15 to 30 per hour;or severe sleep apnea, meaning more than 30 each hour.
4
OSA has been shown to increase the risk for hypertension, pulmonary vascular disease, ischemic
heart disease, cerebral vascular accidents, congestive heart failure, and arrhythmias.[1]
Sleep-related breathing disorders, including obstructive sleep apnea (OSA) and Cheyne-Stokes
respiration with central sleep apnea (CSR-CSA), commonly occur in patients with congestive heart
failure (CHF). In this setting they can have adverse pathophysiologic effects on the cardiovascular
system. OSA may lead to development or progression of left ventricular (LV) dysfunction by
increasing LV afterload through the combined effects of elevations in systemic blood pressure and a
generation of exaggerated negative intrathoracic pressure, and by activating the sympathetic nervous
system through the influence of hypoxia and arousals from sleep.
Abolition of OSA by continuous positive airway pressure (CPAP) can improve cardiac function in
patients with CHF. In contrast to OSA, CSR-CSA is likely a consequence rather than a cause of CHF.
Here, pulmonary congestion causes hyperventilation by stimulating pulmonary irritant receptors.
This leads to reductions in PaCO2 below the apneic threshold during sleep, precipitating
posthyperventilatory central apneas. CSR-CSA is associated with increased mortality in CHF,
probably because of sympathetic nervous system activation caused by recurrent apnea-induced
hypoxia and arousals from sleep.
Treatment of CSR-CSA by CPAP has been shown to improve cardiac function and symptoms of
heart failure. Therefore effective treatments of OSA and CSR-CSA may prove to be useful adjuncts
to the standard pharmacologic therapy of patients with CHF.[2]
5
Review of Literature:
In the Sleep Heart Health Study, comprising 6424 men and women, the presence of OSA (defined as
an apnea-hypopnea index >10/h) conferred a 2.38 relative increase in the likelihood of having HF,
independent of other known risk factors[3].In the second largest case series of patients with HF
undergoing polysomnography, OSA was detected in 37% of 450 and 11% of 81 subjects studied,
with the prevalence of OSA greater in men (38%) than in women (31%).[4]&[5]
The clinical features of OSA in HF are similar to those of OSA patients with normal left ventricular
function. Patients are usually obese and have a history of loud habitual snoring. However, only a
minority complains of excessive daytime sleepiness, suggesting that many patients with HF have
relatively asymptomatic OSA .[5]
In contrast to HF patients without OSA, these disturbances of circulatory control are exacerbated
during sleep, leading to increased myocardial oxygen demand in the setting of recurrent hypoxia,
which can itself directly reduce myocardial contractility.[10]These repetitive stresses place thepatient
with OSA and HF at greater risk of worsening ventricular dysfunction, arrhythmias, and, ultimately,
reduced survival.
OSA also prevents the normal fall in heart rate that accompanies the onset of sleep.[11] When coupled
with marked reflex increases in central sympathetic outflow, which are greater in HF than in
individuals with normal left ventricular function,[12]these marked elevations in afterload and heart rate
increase the metabolic demands of the myocardium in the face of reduced O2 supply, cardiac output,
and coronary perfusion, setting the stage for recurrent nocturnal ischemia and arrhythmias.[13]
Conversely, abolition of OSA can reverse these pathophysiological processes and improve left
ventricular structure and function.[14]&[15]
In a substantial proportion of patients with HF, OSA may play a role in the pathogenesis and
progression of cardiac failure through mechanical, adrenergic, and vascular mechanisms [16]. The aim
of this study is to find out incidence of OSA in HF as mostly it remains undetected in this subset[17]
but its detection and treatment will help reduce the morbidity and mortality[18].
7
Objectives:
To do an observational study of Sleep Apnoea in stable patients of Heart Failure using a clinical
performa, sleepiness questionnaires and limited polysomnography.
8
Materials &Methods:
Study design :
This study is proposed to be a Non- randomized, consequitive, observational study and will be
conducted in the Department of Cardiology at Army Hospital (Research & Referral) which is the
premier tertiary care hospital of the Indian Armed Forces and a super speciality referral centre for
Military Hospitals across the country.
Study methods :
50 patients diagnosed as Stable Heart Failure by the cardiologist at the cardiology OPD of Army
Hospital (R&R), who are at Intermediate to High risk of OSA as per the “STOP-BANG” Sleep
Apnoea questionnaire will be included in the study. Purpose of the study will be explained to the
patients and informed consent will be obtained. Thereafter patients will be assessed clinically and
subjected to an overnight limited Polysomnography (PSG) for confirmation of sleep apnoea.
Study population :
The representative population for this study will be including serving and retired defence personelles
and their families belonging to any race, ethinicity, gender or age throughout the country who are
referred to or first diagnosed at Army Hospital (R&R) from both rural as well as urban background
including both inpatients and outpatients who consented to be a part of the study with a signed
informed consent.
Study size: 50
Ethical Prerequisites:
Scientific Prerequisites:
Inclusion criteria :
1. Sex : Male
3. Patients diagnosed with Stable Heart Failure based on history, clinical examination
and 2D-ECHO by the cardiologist
Exclusion criteria :
11
Investigations to be done :
Blood glucose
Electrocardiograph
Chest x ray
BMI
Echocardiograph
Polysomnography
12
Methodology :
1. The study will be conducted in a tertiary care hospital, Army Hospital (R&R), at
department of cardiology
4. 50 ambulatory male patients with stable heart failure due to systolic dysfunction
(LVEF < 45%) will be selected.
5. The primary investigator or the cardiologist will confirm that they are clinically stable
and on standard therapy, with no change in signs or symptoms of heart failure within
the previous 4 weeks.
6. Polysomnography will be done on these patients to find the presence and type of
sleep apnea.Diagnosis of OSA: Apnea is defined as a >90% reduction in tidal volume
lasting ≥10 s, and hypopnea is a reduction in tidal volume of 50% to 90%, lasting ≥10
s accompanied by ≥3% decrease in oxyhemoglobin saturation (SaO2) or terminated
by arousal from sleep . An OSA disorder is generally defined as the presence of ≥5
episodes of apnea or hypopnea per hour of sleep (i.e., apnea-hypopnea index [AHI])
and when accompanied by either hypersomnolence or at least 2 episodes of choking
or gasping during sleep, recurrent awakenings, unrefreshing sleep, daytime fatigue, or
impaired concentration or memory, constitutes an OSA syndrome.Confirmed by
overnight polysomnography in a sleep laboratory during which sleep architecture,
cardiac rhythm, SaO2, airflow, and thoracoabdominal movements are recorded.
13
Reports of 2D-ECHO.
History:-
General Examination :-
o Ht : cm BMI : Kg/m2
o Wt : kg Temp : F
o PR : bpm BP : mm of Hg
Systemic Examination :-
o Cardiovascular System :
o Respiratory System :
o Gastrointestinal system :
o Nervous System:
15
Investigations :-
HB BUN
TLC CREAT
DLC NA
PLATELET K
TP AST
ALB ALT
ELECTROCARDIOGRA
ECHOCARDIOGRAPHY
POLYSOMNOGRAPHY
Signature of Investigator
___________________
16
STOP YES NO
Do you Snore loudly (louder than talking or loud enough
to be heard through closed doors)?
Do you feel feelTired, fatigued or sleepy during
daytime?
Has anyone Observed you stop breathing while you
sleep?
Do you have high blood Pressure?
BANG YES NO
2
BMI > 35 Kg/m
Age > 50 yrs
Neck circumference > 16 inches(40 cms)
Gender : Male?
TOTAL SCORE
17
References:
1.Sleep Apnoea and Heart Disease, Stroke
2.Sin DD, Logan AG, Fitzgerald FS, et al. Effects of continuous positive airway pressure on cardiovascular
outcomes in heart failure patients with and without Cheyne-Stokes respiration. Circulation 2000;102:61-66
3.Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-
sectional results of the Sleep Heart HealthStudy. Am J RespirCrit Care Med. 2001;163:19–25.
4.Sin DD, Fitzgerald F, Parker JD, et al. Risk factors for central and obstructive sleep apnea in 450 men and
women with congestive heart failure. Am J RespirCrit Care Med. 1999;160:1101–1106.
5. Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81 ambulatory male patients with stable heart
failure: types and their prevalences, consequences, and presentations. Circulation. 1998;97:2154–2159
6.Daly PA, Sole MJ. Myocardial catecholamines and the pathophysiology of heart failure. Circulation.
1990;82(2 suppl):I35–I43
7.Kaye DM, Lambert GW, Lefkovits J, et al. Neurochemical evidence of cardiac sympathetic activation and
increased central nervous system norepinephrine turnover in severe congestive heart failure. J Am
CollCardiol. 1994;23:570–578.
8. Floras JS. Clinical aspects of sympathetic activation and parasympathetic withdrawal in heart failure. J Am
CollCardiol. 1993;22:72A–84A
9. La Rovere MT, Pinna GD, Hohnloser SH, et al. Baroreflex sensitivity and heart rate variability in the
identification of patients at risk for lifethreatening arrhythmias: implications for clinical trials.
Circulation.2001;103:2072–2077
10.Kusuoka H, Weisfeldt ML, Zweier JL, et al. Mechanism of early contractile failure during hypoxia in intact
ferret heart: evidence for modulation of maximal Ca2-activated force by inorganic phosphate. Circ Res.
1986;59:270–282
11.Tkacova R, Rankin F, Fitzgerald FS, et al. Effects of continuous positive airway pressure on obstructive
sleep apnea and left ventricular afterload in patients with heart failure. Circulation. 1998;98:2269–2275.
12.Bradley TD, Tkacova R, Hall MJ, et al. Augmented sympathetic neural response to simulated obstructive
apnea in human heart failure. Clin Sci. 2003;104:231–238.
18
13. Franklin KA, Nilsson JB, Sahlin C, et al. Sleep apnoea and nocturnal angina. Lancet. 1995;345:1085–
1087
14. Malone S, Liu PP, Holloway R, et al. Obstructive sleep apnoea in patients with dilated cardiomyopathy:
effects of continuous positive airway pressure. Lancet. 1991;338:1480–1484
15.Kaneko Y, Floras JS, UsuiK,et al. Cardiovascular effects of continuous positive airway pressure in
patients with heart failure and obstructive sleep apnea. N Engl J Med. 2003;348:1233–1241
16. Bradley TD, Floras JS.Sleep Apnea and Heart Failure. Circulation.2003; 107: 1671-1678
17. Javaheri S, Parker TJ, Wexler L, et al. Occult sleep-disordered breathing in stable congestive
heart failure. Ann Intern Med 1995;122:487-492. Erratum: Ann Intern Med 1995;123:77
18.Javaheri S. Pembrey's dream: the time has come for a long-term trial of nocturnal supplemental
nasal oxygen to treat central sleep apnea in congestive heart failure. Chest 2003;123:322-325
INFORMED CONSENT
Freewill; give my consent to be included as a subject in the clinical study titled “ Study Of Sleep
Apnoea In Patients With Stable Heart Failure ”. I have been informed to my satisfaction, in a language
understood by me, by the investigators of the purpose and nature of the study and of the follow up
including all the investigations to be carried out. I have also been explained about the possible
consequences of the study, which I find acceptable. I am also aware of my right to opt out of the
study at any moment during its course without having to explain my reasons for doing so.
Date: Sign
Patient / NOK/ Relatives