Prognostic Significance of Serum Albumin & Serum Total Cholesterol in Acute Decompensation in Heart Failure
DISSERTATION SUBMITTED TO
THE TAMIL NADU DR.M.G.R MEDICAL UNIVERSITY
IN PARTIAL FULFILLMENT OF THE REGULATIONS FOR THE AWARD OF THE DEGREE OF
M.D (GENERAL MEDICINE) BRANCH – I KAPV. GOVT. MEDICAL COLLEGE & M.G.M.G.H
TIRUCHIRAPALLI
THE TAMILNADU DR.M.G.R MEDICAL UNIVERSITY CHENNAI, TAMIL NADU
MAY 2020
CERTIFICATE FROM THE DEAN
This is to certify that the dissertation titled
“Prognostic significance of serum albumin and serum total cholesterol in Acute Decompensation in heart failure“
is a bonafide research work done by Dr.ANBARASU R under direct supervision and guidance of Prof.Dr.D.NEHRU MD.,DMRD., HOD, Department of General Medicine, in partial fulfillment of the requirements for the award of MD GENERAL MEDICINE degree of The Tamilnadu Dr. M.G.R.Medical University, to be held in May 2020.
Prof.Dr.A.ARSHIYA BEGUM MD., DEAN, K.A.P.V Govt. Medical College, M.G.M.G.H, Trichy.
CERTIFICATE FROM THE HEAD OF THE DEPARTMENT
This is to certify that this dissertation in “Prognostic signifi- cance of serum albumin and serum total cholesterol in Acute De- compensation in heart failure“ is a bonafide research work done by Dr. ANBARASU R, under my guidance, in partial fulfillment of the award of M.D.Degree in General Medicine (Branch-I) by The Tamil Nadu Dr.M.G.R Medical University ,Chennai -600 032.
DR.D.NEHRU MD.,DMRD.,
Professor & Head of Department
Department of General Medicine
KAPV. Govt.Medical College-Trichy
CERTIFICATE FROM THE GUIDE
This is to certify that the dissertation titled “Prognostic significance of serum albumin and serum total cholesterol in Acute Decompensation in heart failure” is a bonafide research work done by Dr.ANBARASU R under my direct supervision and guidance, in partial fulfillment of the requirements for the award of MD GENERAL MEDICINE degree of The Tamilnadu Dr. M.G.R.
Medical University, to be held in May 2020
.
Prof.Dr.D.NEHRU.M.D, DMRD, Professor and Head of the Department, Department of General Medicine, K.A.P.V Govt. Medical College, Trichy.
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Guide & Supervisor sign with Seal.
DECLARATION
I solemnly declare that this dissertation entitled “Prog- nostic significance of serum albumin and serum total cholesterol in Acute Decompensation in heart failure” is a bonafide and genuine re- search work carried out by me at Govt.KAPV.Medical College-Trichy dur- ing the academic year 2017 -2020 under the guidance and supervision of
DR.NEHRU MD.,DMRD.,Professor, Department of Medicine, KAPV. Govt.
Medical College-Trichy.
This dissertation is submitted to The Tamil Nadu Dr.M.G.R Medical University, towards the partial fulfillment of requirement for the award of M.D. Degree in General Medicine (Branch -I).
Place: Trichy Dr. ANBARASU R
Date:
ACKNOWLEDGEMENT
I wish to express my sincere thanks to our respected Dean Prof.Dr.A.ARSHIYA BEGUM MD.,, for having allowed me to conduct this
study in our hospital.
I express my heartfelt thanks and deep gratitude to the guide and Head of the Department of Medicine Prof. DR. D. NEHRU MD., DMRD., for his generous help and guidance in the course of the study.
My sincere thanks to Dr.BALASUBRAMNI M.D, DM, Professor and HOD, Department of Cardiology for their help.
I sincerely thank all Asst. Professors Dr.RAJAMAHENDRAN, and DR.PRABHU M.D, for their guidance and kind help.
My sincere thanks to all my friends and post-graduate colleagues for their whole hearted support and companionship during my studies.
I thank all my PATIENTS, who formed the backbone of this study without them this study would not have been possible.
Lastly, At this juncture I would also want to extend my heartfelt grati- tude to my parents, Mr. Raman & Mrs. Ponnarasi and my wife Mrs.
Sandhiya for the motivation and encouragement extended by them which gave fulfillment to the dissertation work I owe my sincere thanks to all the patients for their kind co-operation throughout the study.
Above all, I thank the ALMIGHTY for gracing me with this oppor- tunity and for giving me courage and good health so that I could carry on my academic course without much hindrance.
LIST OF ABBREVIATIONS
1. ADHF- Acute Decompensated Heart Failure 2. HF- Heart Failure
3. AHFS - Acute Heart Failure Syndrome 4. HFrEF- Heart Failure with a reduced EF 5. HRpEF- Heart Failure with a preserved EF 6. RAAS - Renin-angiotensin-aldosterone system 7. COPD - Chronic Obstructive Lung Disease 8. QOl- Quality Of Life
9. ACEIs - Angietensin Coverting Enzyme Inhibitors 10. ARBs- Angiotensin Receptor Blockers
11. LV - Left ventricular
12. LVH - Left Ventricular Hypertrophy 13. RFT- Renal function tests
14. LFT - Liver function tests
15. TC - Total Cholesterol
16. LDL - Low Density Lipoprotein 17. CCF - Congestive cardiac failure 18. CAD - Coronary artery disease 19. RHD - Rheumatic heart disease 20. CM - Cardiomyopathy
21. DCM - Dilated cardiomyopathy 22. HHD - Hypertensive heart disease 23. ECHO- Echocardiogram
24. ECG - Electrocardiogram 25. DM - Diabetes mellitus 26. HTN - Hypertension
CONTENTS
1. INTRODUCTION 2. AIM OF THE STUDY
3. MATERIALS AND METHODS.
4. REVIEW OF LITERATURE
5. OBSERVATIONS AND ANALYSIS.
6. DISCUSSION
7. CONCLUSION and LIMITATIONS 8. BIBLIOGRAPHY
9. ANNEXURE
1. MASTER CHART 2. PROFORMA
LIST OF TABLES
TABLE NO.
TITLE
1
Age distribution
2 Gender distribution
3
heart rate and blood pressure
4
co-morbidities distribution
5
underlying heart disease
6
Fluid overload distribution
7 chronic medication intake
distribution
8 chest x-ray finding
9
Boston score distribution
10
ejection fraction
distribution11
serum albumin distribution
12
serum cholesterol levels distribution
13hemoglobin and renal parameters distribution
14duration of hospital stay distribution
15
mortality rate
16 Age between survivors vs non-survivors 17
gender between survivors vs non-survivors
18
heart rate and blood pressure between survivors vs non- survivors
19
comorbidities and heart conditions between survivors and non-survivors
20
Boston score - survivors VS non-survivors
21ejection fraction survivors VS non-survivors
22 Distribution of ejection fraction between survivors and non- survivors
23
biochemical parameters between survivors and non- survivors
24
X-ray findings between survivors and non-survivors
25 Mean Duration of hospital stay between survivors andnon-survivors
26 Duration of hospital stay between survivors and non-
survivors
27
hypoalbuminemia and hypocholesterolaemia between survivors and non-survivors
28
duration of hospital stay vs hypoalbuminemia
29duration of hospital stay vshypocholesterolaemia
30serum albumin levels vs other parameters
31cholesterolserum levels vs other parameters
INTRODUCTION:
Acute HF syndromes are one of the most frequent cause of admission to Emergency department in developed countries. This epidemic medical condition primarily affects older patients and carries high hospital mortality rates.
More than 20 million people affected with heart failure. with the prevalence of 2%, which rises with age and the prevalence in > 65 yrs of age is around 6-10%.
Lower in women when compare to men. the increasing trend in HF preva- lence is said to be increased survival rate among patients suffered from causative agents like myocardial ischemia, arrhythmias valvular heart diseases.
Many patients hospitalized with HeartFailure syndrome do not benefit from even after Intensive cardiologist care and multidisciplinary approach and may therefore experience poorer outcomes in major portion of the cases.
A targeted multimarker strategy may, however, be helpful in improving the identification of older patients at high risk of hospital death.
Serum albumin and serum Total Cholesterol are two simple and inexpen- sive markers of malnutrition-inflammation syndrome, recent researches empha-
sizes the importance of serum Albumin & Total cholesterol in identification of pa- tients with ADHF at risk of adverse outcome.
However, it is unknown whether these two biomarkers offer relevant prognostic information incremental to usual prognosticators in patients with acute HF.
Although hypoalbuminaemia occurs in one-third of patients with systolic heart failure (HF)and has been demonstrated to be independently associated with increased risk of death, little is known about the relationship between hypoalbu- minaemia and outcome in HF.
Hypercholesterolemia is a risk factor for development of coronary artery disease (CAD), however, several reports have suggested that low serum choles- terol is associated with a worse prognosis in patients with congestive heart failure (CHF). so serum cholesterol is a double edged sward , when it is very low or very high , associated with inferior outcome in patients with heart failure.
The present study addressed the prognostic relevance of serum albumin and serum TC in the prediction of poor outcome in older patients with ADHF in the form of in hospital mortality & prolongation of hospital stay at admission to a MGM hospital.
AIMS/OBJECTIVES: To address the prognostic relevance of serum albumin and serum TC in the prediction of hospitalization for cardiovascular disease and in hospital death in patients identified as having acute HF at admission
METHODOLOGY: The total duration of study was 1 year.
Design: Is a descriptive study of patients admitted with Acute Decompensation in Heart Failure .
INCLUSION CRITERIA:
1.Age group 18-65yrs
2.All patients with primary diagnosis of ADHF, had symptoms of HF , clinical signs of the same, which responded favourably to intravenous furosemide therapy.
EXCLUSION CRITERIA:
1.Age <18 & >65yrs
2. Acute coronary syndromes by ECG and Echocardiogram, permanent pacemaker pacing, severe arrhythmias (atrial fibrillation, ventricular tachycardia, ventricular fibrillation) , respiratory support, liver cirrhosis, end-stage renal failure requiring dialysis, Nephrotic syndrome and cancer
3. Patients without willingness to participate.
MATERIALS AND METHODS
SOURCE OF DATA:
The present study was done at Mahathma Gandhi Memorial Govt. Hospi- tal attached to K.A.P.V.Govt.Medical College, Tiruchirapalli.
PERIOD OF STUDY:
The study was conducted from December 2017 to December 2018 ETHICAL COMMITTEE APPROVAL:
Approval was obtained from Institutional Ethical Committee.
CONSENT:
Informed consent was obtained from all the participants and their relatives wherever necessary.
PROCEDURE OF STUDY:
In this study, 50 patients who admitted with Acute Decompensation in Heart Failure to the emergency room of Mahathma Gandhi Memorial Govern- ment Hospital,Trichy attached to KAPV Government Medical College were stud- ied for their severity of illness, mortality and duration of hospital stay.
Method of collection of data:
A detailed clinical examination including vital parameters was done to find out the presence of Acute Decompensation in Heart failure, at the time of admis- sion. Patients were included according to the criteria mentioned above, after get- ting informed consent. A written informed consent was taken for participation after explaining the purpose and design of the study to each subject. The patient prior to consent was informed that refusal to participate in the study would not lead to any detrimental consequences or affect the treatment there of.
Obtaining the sample:
Whole blood is collected , at the time of admission and next day morning fasting Sample is sent to laboratory immediately. Various investigations like serum Albumin, Total Cholesterol, urea, creatinine, cardiac enzymes, hemoglobin were done and also electrocardiogram, Echocardiogram are done.
STATISTICAL ANALYSIS:
All the parameters were tabulated. Mean, standard deviation were analyzed using SPSS 20 software. Chi-square test was the test of significance used for qual- itative variables to find the association between them. T test was the test of signifi- cance used for comparing quantitative variables with qualitative variables.
REVIEW OF LITERATURE HEART FAILURE:1,12
Heart failure is a complex clinical syndrome occurring as the end result of many different forms of heart disease. so many different definitions and classifica- tions of heart failure are available but a simple, practical definition is syndrome of heart failure is that it is characterized by typical symptoms such as shortness of breath, exercise limitation and fatigue and clinical signs of peripheral and/or pul- monary congestion, associated with abnormalities of cardiac structure and func- tion1
The current American College of Cardiology Foundation (ACCF)/Ameri- can Heart Association (AHA) guidelines define HF as a complex clinical syn- drome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales.
EPIDEMIOLOGY:1,12,20
more than 20 million people affected with heart failure. with the prevalence of 2%, which rises with age and the prevalence in > 65 yrs of age is around 6-10%. lower in women when compare to men . the increasing trend in HF preva- lence is said to be increased survival rate among patients suffered from myocardial
ischemia, arrhythmias valvular heart diseases. the newer categorization for heart failure is
HF with a reduced EF (HFrEF; formerly systolic failure) HF with a preserved EF (HRpEF; formerly diastolic failure).
Borderline or midrange EF Patients with a LV EF between 40 and 50%
ETIOLOGY:1,12
Condition that produces alteration in LV structure or function can predis- pose to developing Heart failure. Although the etiology of Heart failure in patients with a preserved EF differs from that of patients with depressed EF, there is signif- icant overlap between the causes of these two types. CAD is the predominant eti- ology in development of heart failure men and women which accounts for around 60-75% of total causes of heat failure.
Depressed Ejection Fraction (<40%) 1,12 Coronary artery disease -
Myocardial infarction & Myocardial ischemia.
Chronic pressure overload
Hypertension, Obstructive valvular disease Chronic volume overload
Regurgitant valvular disease Intra cardiac (left- to-right) or Extra cardiac shunting
Chronic lung disease Cor pulmonale
Pulmonary vascular disorders Nonischemic dilated cardiomyopathy
Familial/genetic disorders , Infiltrative disorders Toxic/drug-induced damage
Metabolic disorder Viral
Chagas’ disease
Disorders of rate and rhythm Chronic bradyarrhythmias Chronic tachyarrhythmia
Preserved Ejection Fraction (>40–50%) Pathologic hypertrophy
Primary (hypertrophic cardiomyopathies) Secondary (hypertension)
Aging Endomyocardial disorders Restrictive cardiomyopathy
Storage diseases (hemochromatosis) High-Output States
Metabolic disorders Thyrotoxicosis Nutritional disorders (beriberi)
Excessive blood flow requirements Systemic arteriovenous shunting Chronic anemia
PATHOGENESIS OF HEART FAILURE:1,12
Pathogenesis of two types heart failure is different, in the case of HFrEF the principal event otherwise called index event which started as initial decline in the ejecting capacity of the heart which causes activation of various compensatory mechanism like adrenergic nervous system, RAAS, Cytokine system.
By these compensatory responses patient will be remain asymptomatic for a period of time , at one point this compensatory mechanism itself leads to end or- gan damage and ventricular remodeling, landed in decompensated failure.
This index event may have: Abrupt onset, ( eg; Myocardial infarction), Gradual or insidious onset ( hemodynamic pressure or volume overloading), Hereditary (ge- netic cardiomyopathies).
The continuous action of the neurohormonal and cytokine system leads to series of end organ changes in the cardiac myocardium that process collectively termed as Left ventricular remodeling . and this is is enough to produce heart fail- ure which is independent of the patients neurohormonal status. Because of delete- rious effect of the biologically active molecules and its over expression on the heart and circulation.
COMPENSATORY MECHANISMS:1,12
1. Activation of the Renin-Angiotensin-Aldosterone System (RAAS) - maintaining cardiac output by increased retention of salt and water.
2.Adrenergic nervous system- 1,12 - maintaining cardiac output by in- creased myocardial contractility. & atrial and brain natriuretic peptides (ANP and BNP),
• bradykinin, prostaglandins (PGE2 and PGI2),
• Nitric oxide (NO), reduces peripheral vascular vasoconstriction.
HEART FAILURE WITH REDUCED EF: 12
In failing left ventricle continuous neurohormonal activation and mechani- cal overload result in transcriptional and post transcriptional modification in genes and proteins that regulate the excitation-contraction coupling and cross- bridge in- teraction which disturbs the ability of the myocyte to contract. Because of remod- eling the LV undergoes change in its shape, (ellipse to spherical) leads to an in- crease in LV wall stress, & create the new mechanical overload to the heart.
MECHANICAL DISADVANTAGE OF VENTRICULAR REMODELING:17 Functional MR , Increased wall stress, After load mismatch , Stretch in- duced activation of signal transduction and gene programs. , Episodic Subendo- cardial hypo perfusion, Increased oxygen utilization & Worsening of haemody- namic overloading.
GENETIC BASIS FOR HEART FAILURE:
Left ventricular remodeling is influenced by various factors among those Hemodynamic, Neurohormonal, Epigenetic and genetic factors as well as by nu- merous co-morbid conditions.
Gene pleomorphism is thought to contribute to progression of disease into heart failure by several mechanisms. as this image shows the disease susceptibility genes may increases the risk of developing heart failure after cardiac injury, where as modifier genes can increase and or decrease the effect caused by susceptibility gene. Ultimately gene pleomorphism may alters the response to Heart failure Treatments which is called Therapy modifier genes.
NOMENCLATURE AND DEFINITION:
( LV remodeling )
Alterations in Myocyte Biology
• Excitation-contraction coupling
Myosin heavy chain (fetal) gene expression β-Adrenergic desensitization
Hypertrophy Myocytolysis
Cytoskeletal proteins Myocardial Changes Myocyte loss
Necrosis Apoptosis Autophagy
Alterations in extracellular matrix Matrix degradation
Myocardial fibrosis
Alterations in Left Ventricular Chamber Geometry Left ventricular (LV) dilation
Increased LV sphericity LV wall thinning
Mitral valve incompetence
ACUTE HEART FAILURE:
Defined as new onset or recurrence of symptoms and signs of Heart failure urgent or emergent therapy and resulting in unscheduled care of hospitalization.
Though the terminology is acute , it may present as sub acute pattern with gradual worsening of signs and symptoms, which finally leads to a severity suffi- cient to seek for emergency hospitalization.
other terminologies include
ACUTE HEART FAILURE SYNDROME (AHFS)
ACUTE DECOMPENSATION OF CHRONIC HEART FAILURE (ADCHF) ACUTE DECOMPENSATED HEART FAILURE ( ADHF)
HOSPITALIZATION FOR HEART FAILURE (HHF)
All these terminologies are used interchangeably , though there is no uni- versally accepted single terminology is not there, however here we are using the term ACUTE DECOMPENSATED HEART FAILURE ( ADHF)
ACUTE DECOMPENSATED HEART FAILURE ( ADHF):1
ADHF is a heterogeneous clinical syndrome due to confluence of interre- lated abnormalities of decreased cardiac performance, renal dysfunction, and al-
terations in vascular compliance. Patients with a diagnosis of ADHF is associated with increased morbidity and mortality, which is around 50% of these patients readmitted within 6 months, and around 5% has in hospital mortality and 20%
has long-term cardiovascular mortality at 1 year.
A rapid bedside evaluation categorize heart failure patients into one of four profiles based on presence or absence of congestion and low perfusion:
A, warm and dry;
B, warm and wet;
C. cold and dry;
D, cold and wet.
These simple profiles carry prognostic information and can be used to guide initial treatment of acute decompensated heart failure, and also it shows the severity and nature of the illness and out come of the patient. for example cold pe- ripheries and wet lung that is low perfusion and presence of congestion severe form of illness.
CLINICAL FEATURES:
Symptoms:
Fatigue (due to low output and skeletal muscle abnormalities) & Shortness of breath.
The New York heart association classified the severity of breathlessness in to 4 main classes. as mentioned in the table.
ORTHOPNEA: Dyspnoea occurs in supine position usually later manifestation due to redistribution of fluid in the splanchnic circulation and lower limbs into the central circulation. orthopnoea is more specie symptom of dyspnoea due to cardiac origin.
Paroxysmal nocturnal dyspnoea (PND): 13
is the development of dypnoea when the patient is lying down asleep, wak- ing the patient and usually ( after 1-3 hrs forcing them to sit upright. It results from the development of orthopnoea while the patient is sleeping. it may manifest as cough or wheeze. orthopnoea usually relieved by sitting upright for a while but the Nocturnal dyspnoea will not settle as simple as orthopnoea it takes longer time and make the patient walk for a period.Cardiac asthma is some what similar to PND, is characterized by wheezing secondary to bronchospasm, and it should be differ- entiated from primary asthma and respiratory causes.
Cheyne-Stokes Respiration:
Also Referred To As Periodic Respiration Or Cyclic Respiration, Cheyne-Stokes Respiration Is Present In 40%
Of Patients With A d v a n c e d H f And Usually Is Associated With L o w C a r d i a c Output.
Acute pulmonary edema.
GI symptoms- Anorexia, nausea, and early satiety associated with abdominal pain and fullness due to edema of the bowel wall.
Congestion of the liver and stretching of glisson’s capsule lead to right upper- quadrant pain. Cerebral symptoms - confusion, disorientation, and sleep and mood disturbances,
Nocturia is common problem and may lead to insomnia.
Physical Examination:
General physical examination
• In mild to moderate HeartFailure, the patient is comfortable at rest, with symp- toms of orthopnoea only, but In more severe HF, the patient is dyspnoeic even in siting posture .
• The pulse pressure may be diminished
• Systolic BP may be normal, high or low according to the severity of cardiac failure
• Sinus tachycardia
• Cool peripheries , cyanosed lips and nails
• JVP- may be normal at rest but positive abdomino jugular reflux.
• Giant v waves in JVP indicate the presence of tricuspid regurgitation.
Respiratory Examination:
• Pulmonary crackles due to the transudation of fluid into the alveoli
• Expiratory wheezing (cardiac asthma)
• Pleural effusions resulting from transudation of fluid into the pleural cavities.
• If unilateral they occur more frequently in the right pleural space.
Cardiac findings:1,12
• Cardiomegaly with apical impulse shifted.
• A3rd heart sound (S3) is heard and palpable at the apex due to volume overload
• left parasternal heave due to hypertrophied right ventricle.
• A 4th heart sound (S4) present diastolic dysfunction.
• The murmurs of mitral and tricuspid regurgitation in advanced disease.
Abdomen and Extremities
• Pulsatile liver in systole in tricuspid regurgitation.
• Ascites ,
• symmetrical Peripheral edema in dependent areas.
Cardiac Cachexia: Marked weight loss and cachexia., Indicates a poor progno- sis.
INVESTIGATIONS:1,12
Routine Laboratory Investigations
Complete blood count (CBC), Renal function tests (RFT) , Serum elec- trolytes, Blood sugar values, Liver function tests (LFT), Fasting lipid profile to rule out dyslipidaemia, Thyroid function tests including TSH (Thyroid stimulating hormone) & Urine Routine.
ECG:
No specific changes for heart failure, a normal ECG is observed in only 2%
of case.Common findings include: sinus tachycardia/bradycardia, arrhythmias, left ventricular hypertrophy (LVH), evidence of current or past ischaemia/infarction, and conduction system defects (LBBB, RBBB).
Chest X-ray (CXR):
shows pulmonary congestion and used to diagnose other non-cardiac causes of dyspnoea. Common findings: cardiomegaly, pulmonary congestion with alveo- lar oedema,‘bat’s wings’ and Kerley B lines and pleural effusions.Acute cases shows pulmonary artery dilatation and features of pulmonary congestion. Long standing cases often lack the above classical features.
LV Function Assessment:1
Noninvasive cardiac imaging -two-dimensional (2-D) echocardiogram/
Doppler, It can provide a semiquantitative assessment of LV size and function and also r regional wall motion abnormalities (which indicates prior MI). The left atrial dilation and LV hypertrophy, together with a LV diastolic filling defect pro- vided by pulse-wave and tissue Doppler, is used for the assessment of HFpEF. The 2-D echocardiogram/Doppler is not useful in assessing RV size and pulmonary pressures, which are essential in the management of cor pulmonale.
Magnetic resonance imaging (MRI) provides a comprehensive analysis of cardiac anatomy and function and is the gold standard for assessing LV mass and volumes. uses for accurate imaging modality in patients with HF evaluation, The most useful index of LV function is the EF ejection fraction
EF= stroke volume / end-diastolic volume. EF is easy to measure and easy to conceptualize, so it is widely accepted among clinicians. but the EF has a num- ber of limitations.
EF is normal (≥50%), - systolic function is usually adequate,
EF is significantly depressed (<30–40%), contractility is usually depressed.
Myocardial strain rate imaging using speckle tracking has prognostic value.
Biomarkers:18
• Circulating Natriuretic peptides are valuable markers in identifying people with HF.
• B-type natriuretic peptide (BNP) and N-terminal pro-BNP released from failing heart are fairly sensitive indicators for detecting heart failure with depressed EF
• And also lesser degree of elevation in heart failure cases with preserved EF.
• Levels of Natriuretic peptide rise with age and kidney damage and more elevated in females.
• false negative value may occur in obese
• Other Biomarkers are Troponin T and I , C-reactive protein, TNF recep- tors, Soluble ST-2, Galectin-3 and Uric acid.
Exercise Testing
• Treadmill or bicycle exercise testing valuable for evaluating the need for heart transplantation in severe advanced HF .
• A greatest oxygen uptake (VO2) <14 mL/kg / min associated with bad prognosis.
• VO2<14 mL/kg /min - have better survival with transplantation .
Conditions mimicking heart failure:18
• Obesity
• Chest disease—lung, diaphragm, or chest wall
• Venous insufficiency from lower limbs.
• Drug-induced ankle swelling (like dihydropyridine calcium blockers)
• Drug-induced fluid retention
• Hypoalbuminaemia
• Intrinsic Liver disease
• Pulmonary embolism
• Depression and/or anxiety disorders
• Severe anaemia
• Thyroid disease
• Bilateral renal artery stenosis
MANAGEMENT OF HEART FAILURE:7,1
Nonpharmacologic Management 7
• Limiting sodium intake- reduces diuretic resistance, and avoids fluid overload.
• Regular exercise is an effective method to improving exercise capacity.
• supplements such as creatine, carnitine, l-arginine.
HEART FAILURE WITH PRESERVED EJECTION FRACTION
The first principle is to identify and tackle known precipitants of decompensation.
Precipitating factors of AHFS.
Idiopathic or disease progression
Patient-related factors: Noncompliance with diet/fluids/ medication, Alcohol use.
Medication effects : Nonsterodial anti-inflammatory drugs (NSAIDs) , Calcium- channel antagonists, Class 1A and 1C antiarrhythmics, Thiozolidinedione, Prega- balin.
Cardiovascular disease: ACS, New /uncontrolled arrhythmia, Uncontrolled HTN.
High output states: Hyperthyroidism, Anemia, Febrile illness Pulmonary disease: Pneumonia, COPD/asthma exacerbation
NOVEL TARGETS
phosphodiesterase-5 inhibitor sildenafil, improves filling pressures and right ventricular function
Nitrates, which are nitric oxide donors, they might improve preload, en- dothelial function, coronary perfusion and improved exercise tolerance. ARB with an endopeptidase inhibitor, LCZ696, increases the generation of myocardial cyclic guanosine 3′,5′-monophosphate, which enhances myocardial relaxation, and reduces ventricular hypertrophy.
TREATMENT OF ACUTE DECOMPENSATED HEART FAILURE1,12
GENERAL PRINCIPLES
1) Identification and treatment of the known precipitants of decompensation.
2) Identification and management of medication non-adherence 3) Avoiding the use of medicines like NSAIDS, cardiac stimulants.
4) Treatment of active infection and pulmonary thromboembolism if any.
5) Controlling the heart rate & restoring sinus rhythm 6) Correcting ongoing ischaemia.
7) Stabilisation of hemodynamics.
VOLUME MANAGEMENT
Intravenous diuretics
Intravenous diuretic agents rapidly relieve the symptoms of congestion.
A continuous infusion may be needed when high doses of diuretics are needed or when the effect is suboptimal. Addition of a thiaide diuretic may be need- ed in patients receiving long term loop diuretics and it also has a synergis- tic effect. The intravenous diuretic agents that can be used in acute decom- pensated heart failure are :
• Furosemide: 20 – 200 mg daily ( in severe cases, continuous infusion )
• Torsemide: 10 – 100 mg daily (effective in advanced heart failure)
• Bumetanide: 0.5 – 5 mg daily
• Adjuvant diuretics for augmentation Metolaone, Chorthalidone, Spirono- lactone, Acetao lamide
• Change in weight is used as a marker for adequate dieresis.
Ultrafiltration
Ultrafiltration is an invasive method of fluid removal that supplements the need for diuretics. The advantages of ultrafiltration include controlled rate
moral activity. In view of its electrolyte depletion – sparing effect, this tech- nique is also referred to as aquapheresis. The more severe adverse effects of ultrafiltration are mainly due to renal failure, bleeding complications and in- travenous catheter related complications.
VASCULAR THERAPY 1
Vasodilating Agents
Vasodilators have been used for upstream therapy in the stabilization of patients with acute decompensated heart failure. Vasodilators can be used as first line agents along with diuretics to improve the congestive symptoms in patients with ADHF, in the absence of hypotension. Vasodilators fall into three categories : 1) predominantly venous dilators with subsequent reduction in pre- load, 2) arterial dilators, causing a decrease in afterload, 3) balanced vasodila- tors, with combined action on both arterial and venous systems. Currently available vasodilators include :
Nitroglycerine : 10 – 20 micg/min , upto 200 micg/min . They are potent ven- odilators , causing rapid improvement in pulmonary congestion by producing a rapid decline in pulmonary venous and ventricular filling pressures.
Nitroprusside : 0.3 micg/kg/min , upto 5 micg/kg/min. Sodium Nitroprusside re- quires arterial line placement for titration.
Nesiritide : 2 micg/kg bolus followed by infusion at 0.01 micg/kg/min. It is a recombinant brain-type natriuretic peptide and is a potent vasodilator causing dilatation in both the arterial and venous systems , resulting in significant re- ductions in venous and ventricular filling pressures and mild increase in car- diac output.
Vasopressors
Vasopressors are reserved for patients with marked hypotension with evidence of central organ hypoperfusion. These agents redistribute the cardiac output centrally thereby compromising the peripheral perfusion and increased afterload.
Phenylephrine : a selective alpha 1 receptor agonist with potent direct arterial vasoconstrictor effect and hence used in cases of severe hypotension, particu- larly when the hypotension is due to systemic vasodilation.
Norepinephrine : a potent agonist of the beta 1 and alpha 1 receptor and a weaker agonist of the beta 2 receptor. It causes marked vasoconstriction. Both these agents may lead to end- organ hypoperfusion and tissue necrosis.
IONOTROPIC THERAPY:1 Patients with acute decompensated heart failure have impaired myocardial contractility. Hence, pharmacological agents that increase the concentration of intracellular cyclic AMP through direct and in-
direct pathways serve as positive ionotropic agents. These agents act by in- creasing the intracellular calcium. They augment the cardiac output , improves perfusion and relieves congestion shortly. The various ionotropic agents in use are :
Dobutamine : 2 – 20 micg/kg/min. Tachyphylaxis occurs with infusions longer than 24 to 48 hours because of receptor desensitiation. However, it is the pre- ferred ionotrope in patients with significant hypotension and renal dysfunc- tion.
Milrinone : 0.375 – 0.75 micg/kg/min. It is a phosphodiesterase inhibitor. Since it is renally excreted, dose adjustment is necessary in patients with renal dys- function. Since the mechanism of action of this drug is independent from the adrenergic receptors, there is no receptor down regulation, desensitisation and antagonism by beta blockers.
Levosimendan : 0.05 – 0.2 micg/kg/min. It is a novel agent that improves the cardiac myofilament calcium sensitiation, thereby increasing the myocardial contractility and produces peripheral vasodilation.
Enoximone : 0.25 – 0.75 micg/k g bolus followed by an infusion of 1.25 micg/
kg/min. It is a type IIIA phosphodiesterase inhibitor. Since it is extensively metabolised in liver and excreted renally, dose adjustments are needed in both
hepatic and renal dysfunction. The use of ionotropic agents is associated with increased arrhythmia and hypotension on withdrawal.
POTENTIAL NEW THERAPIES1,12
Vasodilating Agents
Serelaxin : It is a recombinant human relaxin-2 p upregulated in pregnancy with powerful systemic and renal vascular effects. It is tested at 30 micg/kg/
day. Baseline blood pressure should be more than 125mmHg for initiation.
Serelaxin improves dyspnoea and reduces the signs and symptoms of con- gestion.
Natriuretic peptides
Urodilantin : It is a modified pro-atrial natriuretic peptide synthesised and secreted from the distal tubules of kidney that regulates renal sodium ab- sorption and water homeostasis. Ularitide is a synthetically produced urodi- lantin.
Cenderitide : It is another synthetically produced natriuretic peptide that combines the lack of unwanted arterial vasodilation with positive natriuretic effects.
Neurohumoral antagonists
Aliskiren : the first oral direct rennin inhibitor, currently approved for the treatment of hypertension, reduced systemic vascular resistance thereby in- creasing the cardiac index , but had no effect on pulmonary capillary wedge pressure.
Tezosentan : a non-selective endothelin receptor antagonist , has been shown to improve hemodynamics in patients with acute decompensated heart fail- ure.
Angiotensin - II type I receptor beta arrestin – biased ligands : agonizing beta-arrestin mediated favourable pathways while simultaneously antagonizing angiotensin II signalling, are under trial.
Soluble Guanylyl Cyclase Activators: Cinaciguat : shown to improve he- modynamics in patients with acute decompensated heart failure. The mecha- nism of action of this compound is similar to that of organic nitrates.
Ionotropic agents
Omecamtiv Mecarbil : It is a selective myosin activator. It prolongs the ejection period and increases fractional shortening , thereby increasing the contractility without increasing the myocardial oxygen demand. This drug is under con- firmatory trial.
Istaroxime : this new class of drug exerts its action through stimulation of the membrane bound sodium-potassium ATPase and by enhancing the activ- ity of the sarcoplasmic reticulum calcium ATPase type 2a. positive ionotropic effect during systole and rapid sequestration of cytosolic calcium into sar- coplasmic reticulum leading to an enhanced lusitropic effect during diastole.
Stresscopin or Urocortin 2 : It is a peptide hormone of the corticotrophin releasing factor (CRF) family. They bind with high affinity to the corti- cotrophin releasing hormone receptor type 2 , which is highly expressed in the myocardium and in the vascular endothelium, thereby exhibiting potent ionotropic and lusitropic effects.
Renoprotective Agents - Rolofylline : a highly selective adenosine A1 recep- tor antagonist developed to increase the renal blood flow and enhance di- uresis without activating the tubuloglomerular feedback.
HEART FAILURE WITH REDUCED EJECTION FRACTION1,21,22,23
The last 50 years various modalities and changes has arised in the man- agement of HFrEF, that evolved from a diuretics and hemodynamic therapy mod- el. In this regard, these neuro hormonal drugs decreases burden of hospitalizations, and a decline in mortality from both pump failure and arrhythmic deaths
NEUROHORMONAL ANTAGONISM
ReninAngiotensinAldosteroneSystem blockers and beta blockers form the cornerstone of neuro hormonal pharmacotherapy and decline in the symptoms and improvement in cardiac structure and function as well as improvement in QOL.
Researches states that heart failure patients treated with ACEIs shows 23%
reduction in mortality and a 35% reduction in the combination endpoint of mortal- ity and hospitalizations.
Similarly beta blockers shows 35% reduction in mortality on top of the benefit provided by ACEIs alone. However, a group of patients with advanced heart failure may not from these neurohormonal inhibitors fully and even require reduction in dose exposure to maintain clinical stability of that patient with heart failure. so the patient with lower exposure to ACEIs and beta blockers are grouped poor prognosis.
Class Effect and Sequence of Administration:
The beneficial effects of B- blockers are thought to be limited to few drugs such as carvedilol, bisoprolol, and metoprolol succinate—which are the agents tested and proven to improve survival. Beta blockers with intrinsic sympath- omimetic activity (xamoterol) and other agents are not recommended. Patient who are received optimally titrated doses of both ACEIs and beta blockers be estab-
lished in a timely manner have better out come and treatment response rather than which agent is initiated first.
Dose and Outcome
ACEIs achieve greater reduction in hospitalizations at higher tolerable dos- es. similarly B- blockers shows a dose- dependent improvement in cardiac func- tion.
MINERALOCORTICOID ANTAGONISTS1,21,22,23
Aldosterone antagonism is associated with a reduction in mortality in all stages of symptomatic HeartFailure rEF. Elevated aldosterone levels in HFrEF promote sodium retention, electrolyte imbalance, and endothelial dysfunction and may directly contribute to myocardial fibrosis. Selective agent - eplerenone and Nonselective antagonist - spironolactone reduce mortality and hospitalizations.
Raas Therapy And Neurohormonal “Escape” :
Is A Phenomenon That Circulating Levels Of Angiotensin Ii Return To Pre- treatment Levels With Long-Term Acei Therapy In Patients With Hfref. ARBs Blunt This Phenomenon By Binding Competitively To The At1 Receptor.
ARTERIOVENOUS VASODILATION:
Hydralazine reduces systemic vascular resistance and stimulates arterial vasodilatation; Nitrates- transformed in smooth muscle cells into nitric oxide, which stimulates C-GMP production and produces arterial-venous vasodilation.
The combination of hydralazine and nitrates shown to improve survival in HFrEF.
NOVEL NEUROHORMONAL ANTAGONISM1,21,22,23
Angiotensin receptor–neprilysin inhibitor (ARNI) , is LCZ696:, ARB (val- sartan) with an endopeptidase inhibitor (sacubitril), has shown a survival benefit in a large trial versus ARB alone. ARNI become the standard treatment in patients with mild-moderate systolic heart failure when they fail to respond conventional therapy.
HEART RATE MODIFICATION:
Ivabradine is a novel agent, an inhibitor of the funny current in the sinoatri- al node, slows the heart rate without a negative inotropic effect. Ivabradine useful in patients who fail to respond after guideline-based ACEIs, beta blockers, and mineralocorticoid receptor antagonists and with residual heart rate >70 beats/min.
DIGOXIN
Digitalis is cardiac glycosides which exert a mild inotropic effect, attenuate carotid sinus baroreceptor activity, and are sympatho-inhibitory. It should be not-
ed that only the low doses of digoxin are sufficient to achieve beneficial outcomes, importantly higher doses breach the therapeutic safety index and ends with worse outcome. Generally, digoxin is now relegated as treatment for heart failure pa- tients who remain profoundly symptomatic despite optimal neurohormonal block- ing agents and adequate volume control managements.
ORAL DIURETICS
Compensatory Neurohormonal activation results in retention of salt and water. Loop diuretic agents are common one because of their increased poten- cy.Indeed, diuretics therapy are essential to achieve volume control before neuro- hormonal therapy is likely to be well tolerated or titrated.
CALCIUM CHANNEL ANTAGONISTS
Second-generation calcium channel–blocking agents - Amlodipine and felodipine, are effectively reduce blood pressure in Heart Failure with rEF but do not affect morbidity, mortality, or Quality of life. The first-generation agents- ver- apamil and diltiazem, since they may exert negative inotropic effects and destabi- lize previously asymptomatic patients, their use should be discouraged.
STATINS1,21,22,23
Because of their Potent lipid-altering and pleiotropic effects they reduce the major cardiovascular events and improve survival in non–heart failure patients.
Once heart failure is well established, this therapy may not be as beneficial . If statins are used to treat progressive coronary artery disease in patient with heart failure, then they should be advised, but no rationale in giving routine statin therapy in nonischemic heart failure.
INFLAMMATION: Many treatment modalities targeting the inflammatory re- sponse in heart failure patient were tried but none of the trials were shown to bene- fit.
ANTICOAGULATION AND ANTIPLATELET THERAPY:1
HFrEF is many times accompanied by a hypercoagulable state and they are at higher risk of developing thromboembolic events, including stroke, pulmonary embolism, and peripheral arterial embolism.
The use of warfarin is not useful in patients with normal sinus rhythm without a history of thromboembolic events.There was no significant difference in the primary outcome between treatment with warfarin and treatment with aspirin, in patients with reduced LVEF in sinus rhythm, Anyhow recent guidelines support the use of aspirin in patients with ischemic cardiomyopathy rather than anticoagu- lants.
FISH OIL
Long-chain omega-3 polyunsaturated fatty acids (ω-3 PUFAs) has been
shown to be associated with good outcomes in patients with HFrEF. Low EPA lev- els are inversely related to total mortality in patients with HFrEF.
MICRONUTRIENTS
Severe thiamine and selenium deficiency has been described reversible heart failure and malnutrition and diuretics are prime risk factors for thiamine loss.
Supplementation of thiamine in HFrEF with evidence of improved cardiac func- tion but it is restricted to chronic heart failure states and does not in the ADHF phenotype. Routine supplementation or testing for thiamine deficiency not rec- ommended.
ENHANCED EXTERNAL COUNTERPULSATION (EECP):1,21,22,23
Graded external pneumatic compression at Peripheral lower extremity us- ing high pressure is administered in 1-h sessions for 35 treatments (7 weeks) and It reduces extend time to exercise-induced ischemia and angina symptoms in patients with coronary artery disease.
EXERCISE
Regular exercise is an effective method to improving exercise capacity and also reduce hospitalization and mortality.
MECHANISM OF HEPATIC DYSFUNCTION IN HEART FAILURE 14,15,16 Heart failure causes: There are two important mechanism proposed for liver dysfunction in patient with heart failure , Decreased blood supply to liver & In- creased hepatic venous pressure.
Long standing venous stasis leads to thrombus formation in sinusoids and venules which has fibrogenic tendency leading to regional fibrosis in liver.
Reduced blood supply to liver is also important in causing necrosis of cells.
HUMAN ALBUMIN:31,32,33,34
Biochemical and Physiological Properties of Human Serum Albumin2
human serum Albumin is protein with 65 KDa molecular weight, which contributes to around 50% of total proteins in the plasma . every day in normal healthy individuals 10-15 g of albumin is produced in liver which was released in
the circulation. albumin synthesis is affected by Nutritional intake , colloid oncot- ic presser changes , insulin and systemic or chronic infection or inflammation. and the mechanism of catabolism of serum albumin was not fully understood it is thought that to occur in all tissues , particularly in the skin , muscles and liver. 2 the normal concentration of serum albumin is 3.5- 5 g/dl. this value may vary lab to lab, small decline ay occur in elderly populations. Our lab reference value is 3.5-5.5 g/dl. the plasma concentration depends on various factors like albumin production , rate of degradation and the distribution and exogenous albumin loss.
Physiological properties:
Binds with various endogenous and exogenous molecules and act as trans- port ao carrier molecule, It has role in antioxidant mechanism
Anti inflammatory properties 33,34
Cardiology specific properties include major contribution to mainatance of plasma oncotic pressure hypoalbuminemeia is a common finding in patient with heart failure around 18-89% of population. it is hypothesized to occur by malnutri- tion , inflammation and cachexia. other reasons in heart failure are haemodilution,4 liver disorders, protein losing enteropathy, and increased trans capillary leakage and nephrotic syndrome.
The forces that govern fluid balance across the capillary membrane are summarized by the modified Starling equation. Jv5LxAx1⁄2ðCHP IHPÞ bxðpc pifÞ
where Jv is the transcapillary filtration rate, L is the micro- vascular hydraulic conductivity, A is the microvascular ex- change vessel surface area, CHP is the in- tracapillary hydrostatic pressure, IHP is the interstitial hydrostatic pres- sure, ß is the protein reflection coefficient, pc is the plasma oncotic pressure, and pif is the interstitial oncotic pressure.
In hypoalbuminemia the starling forces produces a shift of fluid from in- travascular space to interstitial space which causes activation of baroreceptor mechanism and leads to Na and H2o retention. shifting of fluid from the intravas- cular space to intertitial space results in peripheral edema. but in case of occur- rence of pulmonary edema the mechanism will be little different, the lymphatic drainage of the lung ha sthe extra vascular lung water , and increase in PCW pres- sure which interfere with the reabsorption of fluid from interterm and alveoli.2 Hypoalbuminemia as an Additive Cause of Pulmonary Edema2
According to Starling’s law, hypoalbuminemia would be expected to facili- tate pulmonary edema formation. This theoretical consideration is confirmed by experimental and clinical evidence. Guyton and Lindsay modified left atrial pres-
sure and plasma protein concentration in anesthetized dogs. A critical increase in left atrial pressure higher than 24 mm Hg was associated with the development of pulmonary edema. A reduction of 50% in plasma protein concentration lowered the hemodynamic threshold of extravascular lung water accumulation. Pulmonary edema formation began when left atrial pressure rose above 11 mm Hg, and the rate of extravascular water accumulation was proportional to the rise in left atrial pressure.
Hypoalbuminemia in heart failure:8,9
Hypoalbuminemia is common problem in patients with heart failure which is around 25%, and sometimes even more common in the elderly population or frail.In acute decompensated heart failure (ADHF), hypoalbuminemia may aggra- vate the peripheral edema and pumonary congestion at lower left atrial pressures.
Similarly Hypoalbuminemia has also been associated with incident wors- ening renal function (WRF) during decongestive therapy for Acute Decompensat- ed Heart Failure. It is because of inability to maintain volume status and lead to intravascular volume depletion and decreased renal perfusion.
Furthermore, hypoalbuminemia in ADHF is associated with a higher rates of poor outcomes, and its prognostic significance may be more pronounced in pa- tients with reduced left ventricular EF.
There is one hypothesis that lower baseline albumin levels is associated with incident Worsening Renal Failure, worsening heart failure (WHF), and less response to decongestive therapies. Another alternative explanation is that risk fac- tors associated with development of Heart Failure are also affects serum albumin biochemical profile.
These observations suggest an interesting facts of serum albumin as a strong surrogate marker for incident Heart Failure in the elderly, Sr.Albumin that possibly integrates both known and unexplored pathways.
Further research into antithrombotic or antioxidant mechanisms, oxidative stress due to the nitric oxide reservoir property of albumin, or other mechanisms may have great role in future therapeutic interventions of Heart failure patients.
TOTAL CHOLESTEROL:31,35
Cholesterol (chole – bile , sterol – solid )is a precursor of bile acids and steroids hormones .it has an important structural role in cell membranes .It is syn- thesized mainly in liver but also in all other tissues .
Cholesterol and dietary triglycerides are absorbed from intestine is trans- ported by chylomicrons to liver whereas VLDL carries endogenous triglycerides from liver to blood TG content of chylomicrons more than the cholesterol content .in the wall of the blood vessel . TG contained in the chylomicrons are me- tabolized by lipoprotein lipase and free fatty acid so formed are utilized by various tissues like fat and muscle . Hepatic lipase present on the surface of liver metabo- lizes remaining TGSs and the chylomicrons remnant ( only cholesterol) are taken up by the liver . net result of this process is transport of dietary cholesterol to liver and free fatty acid to fat and muscle .
when TG production in the liver increases ,VLDL is formed and is released in the circulation .TGs are metabolized by LIPOPROTEIN LIPASE and VLDL is converted to IDL and then to LDL. LDL is taken up by the liver through LDL re- ceptor . HDL is formed by taking cholesterol from tissues and helps in the trans-
port of this cholesterol to the liver ( reverse cholesterol transport ). Thus HDL is-
good cholesterol and LDL IDL & VLDL are bad cholesterols
Cholesterol is synthesized in the body entirely from acetyl CoA. Meval- onate is formed from acetyl C oA molecules by the enzyme HMG CoA reduc- tase. It is the rate limiting step in cholesterol synthesis . It is further transformed into isoprenoid and then to squalene . squalene molecules undergo cyclization to form steroid lanosterol, which after the loss of 3 methyl groups forms cholesterol.
Inherited defects of cholesterol in lipoprotein metabolism lead to hypo or hyper lipoproteinemia . systemic conditions like chronic kidney disease DM , hypothy- roidism are also associated with hyperlipoproteinemia .
Apart from hereditary factors , environmental and dietary factors also play an important role in determining serum cholesterol . saturated fatty acid should replaced by polyunsaturated and monounsaturated fatty acids . examples for PUFA include corn oil and sunflower seed oil. Olive oil contain high levels of MUFA. Reason for beneficial effect of PUFA in cholesterol metabolism is un- known . It increases the number of LDL receptors compared to structural fatty acids . LDL and VLDL are main the main atherogenic lipoproteins since it con- tains more amount of cholesterol.
When diet and lifestyle modification fail , drugs will reduce serum choles- terol. First line drugs include Statins , bile acid binding resins and intestinal cho- lesterol absorption inhibitors whereas second line drugs include fibrates and niacin.
Though high concentration of serum cholesterol associated with incensed risk of coronary artery disease and it indicates worst prognosis .On the other hand patients with congestive heart failure whose nutrition was poor had low serum cholesterol and it shows worst outcome. so serum cholesterol is a double edged sword , when it is very low or very high , associated with inferior outcome in pa- tients with heart failure.
RESULTS
Table 1: Age distribution of the study sample (n=50)
Mean age: 54.7 years Standard deviation: 6.72 Minimum: 40 years Maximum: 65 years
Age group Frequency Percentage
40 to 45 years 4 8.0
46 to 50 years 10 20.0
51 to 55 years 12 24.0
56 to 60 years 14 28.0
61 to 65 years 10 20.0
Total 50 100.0
No of patients
0 4 7 11 14
Years
40-45 46-50 51-55 56-60 61-65
10 12 14
10 4
Table 2: Gender distribution of the study sample (n=50)
Comments: About 70% were males and male preponderance in heart failure is ob- served.
Gender Frequency Percentage
Male 35 70.0
Female 15 30.0
Total 50 100.0
Male Female
Table 3: Descriptive statistics of heart rate and blood pressure (n=50)
Parameter Heart rate
(beats/min) Systolic BP
(mmHg) Diastolic BP (mmHg)
Mean 100.66 114.04 70.00
Std. Deviation 18.398 14.139 10.102
Minimum 56 90 60
Maximum 142 160 100
0 40 80 120 160
Minimum Mean Maximum
heart rate SBP DBP
Table 4: Distribution of the study sample according to co-morbidities (n=50)
*Not mutually exclusive
co-morbidities* Frequency Percentage
Diabetes 8 16.0
CKD 2 4.0
CVA 1 2.0
HTN 10 20
No of patients
0 5 10 15 20
Co morbidities
20
2 1 8
DM CKD CVA HTN
Table 5: Distribution of the study sample according to underlying heart disease (n=50)
*Not mutually exclusive
Underlying heart disease* Frequency Percentage
CAD 45 90.0
COPD/ Cor pulmonale 5 10.0
Hypertension/LVH 10 20.0
DCM 13 26.0
Anaemia 1 2.0
No of patients
0 12.5 25 37.5 50
Underlying Herat disease
1 10 13
5 45
CAD COPD HTN DCM Anaemia
Table 6: Distribution of the study sample according to Fluid overload (n=50)
Comments: 82% of the subjects had fluid overload.
Fluid overload Frequency Percentage
No 9 18.0
Yes 41 82.0
Total 50 100.0
Yes No
Table 7: Distribution of the study sample according to chronic medica- tion intake (n=50)
Comments: 96% of the subjects were taking medications for a long time
chronic medication
intake Frequency Percentage
No 2 4.0
Yes 48 96.0
Total 50 100.0
Yes No
. Table 8: Distribution of the study sample according to chest x-ray finding (n=50)
Comments: Half of the subjects had had cardiomegaly while 20% had pul- monary edema.
chest x-ray finding Frequency Percentage
Cardiomegaly 29 58.0
Pulmonary edema 20 40.0
Non-specific 4 8.0
Total 50 100.0
8%
38%
55%
Cardiomegaly Pulmonary edema Nonspecific
Table 9: Distribution of the study sample according to Boston score (n=50)
Mean score: 8.88 Standard deviation: 1.745
Minimum: 4 Maximum: 12
Comments: About 82% had a higher boston score indicating a definite heart failure.
Boston score Frequency Percentage
Definite (8-12) 41 82.0
Possible (5-7) 8 16.0
Unlikely (<4) 1 2.0
Total 50 100.0
Unlikeley(<4) Possible(5-7) Definite(8-12)
Table 10:Distribution of the study sample according to EF (n=50)
Mean score: 37.92% Standard deviation: 5.746%
Minimum: 25% Maximum: 55%
Comments: 38% & 28% had moderate and severe systolic dysfunction, respective-
Ejection fraction (%) Frequency Percentage
Normal (55) 1 2.0
Mild systolic dysfunction (40-54) 16 32.0 Moderate systolic dysfunction (35-39) 19 38.0 Severe systolic dysfunction (<35) 14 28.0
Total 50 100.0
No of patients
0 5 10 15 20
EF %
14 19
16
1
Normal 55 Mild 40-54 Moderate 35-39 Severe <35
Table 11: Distribution of the study sample according to serum albumin levels (n=50)
Mean score: 3.26 g/dl Standard deviation: 0.521 g/dl Minimum: 2.0 g/dl Maximum: 4.5 g/dl Comments: About 70% of subjects had Hypoalbuminemia.
Serum albumin levels (grams/dl) Frequency Percentage
Normal (≥3.5) 15 30.0
hypoalbuminemia (<3.5) 35 70.0
Total 50 100.0
No of patients
0 10 20 30 40
35 15
Normal Hypoalbuminemia
Table 12: Distribution of the study sample according to serum choles- terol levels (n=50)
Mean score: 162 mg/dl Standard deviation: 26.37 mg/dl Minimum: 112 mg/dl Maximum: 202 mg/dl Comments: Only 16% of subjects had Hypocholesterolaemia.
Serum cholesterol levels (mg/dl) Frequency Percentage
Normal (≥135) 42 94.0
Hypocholesterolaemia (<135) 8 16.0
Total 50 100.0
No of patients
0 12.5 25 37.5 50
Normal Hypocholesterolemia
Table 13: Descriptive statistics of hemoglobin and renal parameters (n=50)
Parameter Hemoglobin
(gms/dl) B.Urea
(mg%) S.creatinine (mg%)
Mean 11.522 41.04 1.288
Std. Deviation 1.8984 11.817 0 .6193
Minimum 5.4 25 0.8
Maximum 16.6 84 3.9
0 40 80 120 160
Urea
Minimum Mean
Maximum
0 1.5 3 4.5 6
Creatinine
Minimum Mean
Maximum
0 10 20 30 40
Hb Minimum Mean Maximum
Table 14: Distribution of the study sample according to duration of hos- pital stay (n=50)
Mean score: 6.4 days Standard deviation: 2.5 days Median: 5.5 days IQR: 5 to 8 days
Comments: The medial duration stay was around 6 days.
Duration of hospital stay Frequency Percentage
<5 days 25 50.0
6 to 10 days 20 40.0
>10 days 5 10.0
Total 50 100.0
No of patients
0 7.5 15 22.5 30
Days
5 20
25
<5 Days 6-10 Days >10 Days
