Clinical Journal of Hypertension · respectively. A higher proportion of patients with uncontrolled T2DM and HTN reported depression than those with controlled T2DM and HTN (T2DM:

ClinicalJournal of Hypertension

EDITOR-IN-CHIEF

Dr. Siddharth N. Shah

JANUARY-MARCH 2019 § VOL. NO. 3 § ISSUE NO. 3Mumbai § Published on 15th of January, 2019

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Editor-in-Chief

Siddharth N. Shah

Associate Editors

Falguni Parikh § Shashank R. Joshi § N.R. Rau § G.S. Wander

Assistant Editors

Nihar P. Mehta § Dilip Kirpalani

Editorial Board

M.M. Bahadur § Amal K. Banerjee § R.K. Bansal § A.M. Bhagwati § Aspi R. Billimoria Shekhar Chakraborty § R. Chandnui § R.R. Chaudhary § M. Chenniappan Pritam Gupta § R.K. Jha § Ashok Kirpalani § Girish Mathur § Y.P. Munjal

A. Muruganathan § K.K. Pareek § Jyotirmoy Paul § P.K. Sashidharan N.P. Singh § R.K. Singhal § B.B. Thakur § Mangesh Tiwaskar § Trupti Trivedi § Agam Vora

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Printed, Published and Edited by Dr. Siddharth N. Shah on behalf of Hypertension Society India, Printed at Shree Abhyudaya Printers, Unit No. 210, 2nd Floor, Shah & Nahar Indl. Estate, Sitaram Jadhav Marg, Sun Mill Compound, Lower Parel, Mumbai 400 013 and Published from Hypertension Society India. Plot No. 534-A, Bombay Mutual Terrace, Sandhurst Bridge, 3rd Floor, Flat No.12, S.V.P. Road, Grant Road, Mumbai 400 007.

Editor : Dr. Siddharth N. Shah

3

Vol. 3 • Issue No. 3 • January-March 2019

Official Publication of Hypertension Society IndiaEditor-in-Chief: Siddharth N. Shah

clinical

Journal of Hypertension

EDITORIALSleep Disordered Breathing Nimish Shah .............................................................................................................................................................................................................................. 5

ORIGINAL ARTICLEECG Left Atrial Abnormality: A Marker of Stroke Prediction in Hypertension Harsh Kaushal, Darshan Mehra, RR Chaudhary .............................................................................................................................................................. 7

REVIEW ARTICLEObstructive Sleep Apnea and Hypertension: A Reciprocal Menace DP Singh, Abhishek Kumar Tiwari .................................................................................................................................................................................... 11

CASE REPORTBiochemically Negative Pheochromocytoma - 2 Case Reports Nandini Prasad, Abilash Nair, Geena Susan George, Jabbar PK, C Jayakumari ......................................................................................................20

The Immediately Evident may be Insufficient Vishnumoorthy, Smitha Bhat, Sudeep K ..........................................................................................................................................................................22

ABSTRACTSPrevalence of Depression in Indian Patients with Type-2 Diabetes Mellitus and / or Hypertension: DEPTH Study R Lalwani, JD Shah, T Chatterjee, PN Rao, S Erande ..................................................................................................................................................... 6

Prevalence of Hypertension and Co-morbidities in Young Diabetics in India U Ayyagari, B TS, V S, D CS, J Gopal, A Behl, KG Seshadri .......................................................................................................................................17

Retrospective Study to Evaluate Efficacy and Safety of Azilsartan in Diabetic Hypertensive Patients from Hospital in Gujarat MA Agarwal, D Agarwal, DC Raval, DU Petare, DYS Petare ....................................................................................................................................29

The Effect of Hypertension and Diabetes Mellitus on White Matter Changes in MRI Brain: A Comparative Study between Patients with Alzheimer’s Disease and an Age-matched Control Group Uma Sundar, Abhilasha A Manwatkar, Anagha R Joshi, Prashant Bhandarkar ........................................................................................................29

Pulmonary Hypertension in Patients with End Stage Renal Disease on Maintenance Hemodialysis-A Cross- sectional Study Narinder Pal Singh, Arushi Nautiyal, Ajay Karol, Neeru P Aggarwal, Gaurav Minocha, Anish Kumar Gupta ................................................30

A Randomized, Double-blinded, Controlled, Multicentre Phase III Study to Evaluate the Efficacy and Safety of Telmisartan/Amlodipine/Hydrochlorothiazide Compared to Telmisartan/Hydrochlorothiazide in Patients with Essential Hypertension JS Hiremath, K Chokalingam, G Mathan, P Naveen Chander Reddy, A Sharma, S Dhawan, A Toppo ............................................................30

ANNOUNCEMENTSHSI Nomination for the post of Executive Committee for the year 2019-2020 ...............................................................................24

Abstract Submission Form of 28th National Conference on Hypertension.........................................................................................25

28th Annual Conference of Hypertension Society of India & 1st International Kidney and Hypertension Conference ..31

Contents

4 Clinical Journal of Hypertension | January-March 2019 | Vol. No. 3 | Issue No. 3

Governing Body

Hon. PatronsAspi R. Billimoria (Mumbai) • N.R. Rau (Udupi)

President Executive Chairman P. K. Sasidharan (Calicut) Siddharth N. Shah (Mumbai)

President - Elect Past President Ashok Kirpalani (Mumbai) Shashank R. Joshi (Mumbai)

Vice PresidentsR. Chandni (Calicut) • R.R. Chaudhary (Patna)

Secretary General Jt. Secretaries B.R. Bansode (Mumbai) Santosh B. Salagre (Mumbai) • Anita Jaiswal – Ektate (Mumbai)

TreasurerAshit M. Bhagwati (Mumbai)

Chairman: Research CommitteeGurpreet S. Wander (Ludhiana)

Editor : Clinical Journal of HypertensionSiddharth N. Shah (Mumbai)

Chairman: Epidemiology CommitteeA. Muruganathan (Tirupur)

MembersD.P. Singh (Bhagalpur) • Dilip Kirpalani (Mumbai) • Nihar P. Mehta (Mumbai)

Shibendu Ghosh (Kolkata) • K.G. Sajeeth Kumar (Kozhikode) • R.K. Jha (Indore) • P.K. Sinha (Gaya)


1Consultant-Pulmonary & Sleep Medicine, Jaslok Hospital & Research Centre, Mumbai, Maharashtra; Sir H.N. Reliance Foundation Hospital, Mumbai, Maharashtra

Sleep Disordered Breathing

Nimish Shah1

EDITORIAL

agulability which are common underlying risk factors for cardiovascular diseases. The review article in this issue by Singh and Tiwari highlights the mechanisms of the same along with outcomes with treatment and lifestyle modifications.The gold standard diagnostic test for OSA is a nocturnal polysomnography, which is available as a home test as well as in-hospital study. Other limited studies are also available and can be done for a diagnosis of OSA. With increased awareness amongst physicians, especially in cardiovascular and metabolic clinics, we hope that the tests and eventually pick-up rate for this condition will improve and reduce the co-morbidities associated with this condition.Effective treatments are available with continuous positive airway pressure (CPAP) therapy and mandibular advancement devices (MAD). However, there is limited long-term adherence to therapy, as CPAP and MAD require continuous usage to avoid recurrence of the symptoms and adverse morbidities.Recently, the INSPIRE®1 device which is an implantable hypoglossal nerve stimulator to stimulate the pharyngeal dilator muscles of the upper airway during sleep has been approved by several healthcare systems. Newer advances with a non-invasive approach are being developed as alternative to CPAP failure therapy (TESLA2). In terms

Sleep disordered breathing is one of the most under recognized, under diagnosed disorders which has multiple co-morbidities which are well evidenced.The incidence and prevalence of OSA (obstructive sleep apnoea) is not well evidenced in the Indian context and needs larger studies to gauge the burden of OSA in the Indian population. We however know that OSA is a global health problem of increasing prevalence. With the incidence of hypertension and diabetes on the rise, along with the increasing body mass index (BMI) of our population, the incidence and prevalence of OSA is only likely to increase.In 2010 the World Health Organisation (WHO) published it’s first ever report on non-communicable diseases which showed that physical inactivity was one of the leading cause of obesity and hence morbidity regarding the same especially in the lower and middle-income countries. With our change in lifestyle, fingertip technology and access this problem is only due to multiply.Evidence has shown that reduced sleep opportunity as well as OSA causes oxidative stress, increased inflammation, endothelial dysfunction, dyslipidaemia and hyperco-


Prevalence of Depression in Indian Patients with Type-2 Diabetes Mellitus and / or Hypertension: DEPTH StudyR Lalwani1, JD Shah2, T Chatterjee3, PN Rao4, S Erande5

ABSTRACTBackground and Aims: Patients wife type-2 diabetes mellitus (T2DM) and hypertension (HTN) are at increased risk of depression which eventually worsens fee symptom perception, negatively impact self-care behaviour and produce detrimental effect on clinical outcomes. Hence fee objective of this study was to determine fee prevalence of depression in Indian patients wife controlled and uncontrolled T2DM and/or HTN. The association of depression wife socio-demographic profile and clinical risk factors was also assessed. Materials and methods: About 1829 eligible patients with T2DM and/ or HTN were included in this cross-sectional clinico-epidemiological pan India study conducted across 54 sites in India. The primary outcome measure was to determine the prevalence of depression in T2DM, HTN and T2DM + HTN patients. The other outcome measures were to identify the association between depression and patients’ demographic profile, socioeconomic status, lifestyle parameters, co-morbidities, disease duration, anxiety, and clinically diagnosed insomnia.Results: All 1829 patients (T2DM: 631; HTN: 573; T2DM+HTN: 625) completed the study. The prevalence of depression in T2DM, HTN and T2DM+HTN patients was 37.9%, 46.1 % and 48.4%, respectively. A higher proportion of patients with uncontrolled T2DM and HTN reported depression than those with controlled T2DM and HTN (T2DM: 31.1% vs. 6.8%; HTN:33.8% vs. 12.3%). Association between higher monthly family income and socioeconomic status with depression was evident in patients with T2DM and HTN (p<0.05). There was a significant association between anxiety and depression across all indications (p<0.0001). The most common comorbidity reported was dyslipidemia (T2DM: 24.22%, HTN: 14.87%, T2DM+ HTN: 27.3%). Among the complications, angina (13.01%) and heart failure (11.15%) were most common in HTN patients, diabetic neuropathy (13.35%) in T2DM and angina (12.50%) and diabetic foot ulcers (2.30%) in T2DM+HTN patients. There was no significant association between depression and comorbidities/complications in T2DM and/or HTN cases.Conclusion: Depression is quite prevalent among Indian patients with T2DM and/or HTN. Our results indicate that patients with controlled T2DM/HTN have less odds of depression. A direct significant association between depression and various socio-demographic variables was also noted in this study. Further, patients with depression tend to have high chance of comorbid anxiety.

1P.G. Medical Centre, Delhi; 2Sharada Medical Nursing, Ahmedabad, Gujarat; 3Dr. Tapas Chatterjee Consultancy, Kolkata, West Bengal; 4Icon Hospital, Hyderabad, Telangana; 5Akshay Hospital, Pune, Maharashtra

of treatment, we are indeed headed towards exciting times and hope to change the outcome of the disease and it’s co-morbidities in totality.

RefeRenCeS1. Upper-Airway Stimulation for Obstructive Sleep

Apnea Strollo et al. N Engl J Med 2014; 370:139-149 DOI: 10.1056/NEJMoa1308659.

2. Randomised sham-controlled trial of transcutaneous electrical stimulation in obstructive sleep apnoea Pengo et al. Thorax doi:10.1136/thoraxjnl-2016-208691.

ABSTRACT


1Resident, 2Associate Professor, 3Professor, Department of Medicine, Rohilkhand, Medical College and Hospital, Bareilly 243006, Uttar Pradesh

Ecg Left Atrial Abnormality: A Marker of Stroke Prediction in Hypertension

Harsh Kaushal1, Darshan Mehra2, RR Chaudhary3

ORIGINAL ARTICLE

ABSTRACTBackground: Stroke is a major cause of mortality and morbidity worldwide and is the second cause of mortality. Hypertension is regarded as the single most important risk factor for stroke; cardiac disease, atherosclerosis, diabetes mellitus, cigarette smoking, obesity and dyslipidemia are reported to be strongly associated with stroke Electrocardiographic (ECG) left atrial abnormality has been associated with stroke independently of atrial fibrillation (AF), suggesting that atrial thromboembolism may occur in the absence of AF. Present study focus on that abnormal PTFV1 (P Terminal Force in precordial lead V1) is predictive of atrial fibrillation, stroke, heart failure hospitalizations and death in general population as well as in patients with prior myocardial infarctionMethod: Case-cohort analysis at Rohilkhand Medical College in Bareilly, a prospective cohort study of stroke risk factors. P-wave terminal force in lead V1 (PTFV1) was manually measured from baseline ECGs of participants in sinus rhythm who subsequently had ischemic stroke (N = 144) and a randomly selected sub cohort without stroke (N = 310). Weighted Cox proportional hazards models were used to examine the association between PTFV1 and stroke etiological subtypes while adjusting for baseline demographic characteristics, history of AF, heart failure, diabetes, hypertension, tobacco use, and lipid levelsFindings: Participants with ischemic stroke had a significantly higher PTFV1 than those in the sub cohort. In an unadjusted model, PTFV1 was associated with a higher risk of ischemic stroke. This association did not substantially change after inclusion of potentially confounding or mediating covariates including a history of AF. Associations between PTFV1 and stroke were unchanged or stronger when we entirely excluded participants who had a baseline history of AF or were diagnosed with AF during follow-up.Conclusion: The value of PTFV1 in predicting ischemic stroke documented by this study conducted in middle-aged hypertensive patients with ECG-LVH needs to be confirmed in larger studies representative of unselected hypertensive population.


InTRODUCTIOnStroke is a major cause of mortality and morbidity worldwide and is the second cause of mortality accounting for approximately 20% of all deaths in women and 15% in men worldwide. Hypertension is regarded as the single most important risk factor for stroke; cardiac disease, atherosclerosis, diabetes mellitus, cigarette smoking, obesity and dyslipidemia are reported to be strongly associated with stroke.1

International hypertension guidelines recommend cardiovascular risk stratification in the population based on blood pressure (BP) levels, modifiable and nonmodifiable risk factors, cardiac and extracardiac organ damage, diabetes mellitus and established cardiovascular or renal disease. 2,3

As for the assessment of target organ damage, recent ESH/ESC Guidelines re-emphasize the role of ECG as first-line examination for detection of subclinical cardiac damage. ECG left ventricular hypertrophy (LVH) indeed is a powerful marker of increased cerebrovascular as well as cardiac mortality and morbidity in the general and hypertensive population.4

Several longitudinal studies identified left atrial size as an independent predictor of incident atrial fibrillation , stroke, congestive heart failure and cardiovascular death.5,6 Furthermore, the extent of dilatation has been linked to severity of ischemic stroke or pattern of ischemic lesions in cross-sectional analyses conducted in patients with nonvalve atrial fibrillation; left atrial size, indeed, turned out to be directly related to the degree of neurologic deficit evaluated according to the National Institutes of Health Stroke Scale. In the majority of these studies, anatomical left atrial abnormalities were investigated by assessing echocardiographic anteroposterior left atrial diameter by M-mode technique under two-dimensional (2-D) control or, less frequently, by measuring left atrial volume on 2-D imaging.7

Prospective studies have shown that abnormal PTFV1 (P Terminal Force in precordial lead V1) is predictive of atrial fibrillation, stroke,

heart failure hospitalizations and death in general population as well as in patients with prior myocardial infarction. This marker was independently associated with sudden cardiac death in individuals with and without prior cardiovascular events, even after adjustment for traditional coronary risk factors. Notably, the risk of sudden cardiac death associated with abnormal PTFV1 exceeded the risk of nonfatal coronary heart disease, heart failure and stroke.8,9

Atrial fibrillation is found in a third of all ischemic strokes, even more after post-stroke atrial fibrillation monitoring.10 The patients with a diagnosis of non-rheumatic atrial fibrillation, without any treatment apart from aspirin in some showed a higher percentage of stroke.11 Left atrial size appears to be an important risk factor, and the control of blood pressure and glucose may be important in preventing the development of AF.12 In an elderly, population-based sample, left atrial enlargement, increased left ventricular wall thickness, and reduced left ventricular fractional shortening were predictive of risk for nonrheumatic atrial fibrillation.13 Study showed that a larger LA volume was associated with a higher risk of AF in older patients. The predictive value of LA volume was incremental to that of clinical risk profile and conventional M-mode LA dimension.14 P Terminal Force (PTF) ≥0.04 mm·s is a relatively common finding in a 12-lead ECG of middle-aged subjects. PTF ≥0.06 mm·s is associated with increased risk for atrial fibrillation and death in the general population.15 The value of P-wave morphology extends beyond cardiac arrhythmias associated with atrial conduction delay and can be used for prediction of clinical outcome of a wide range of cardiovascular disorders, including ischemic heart disease and congestive heart failure.16 a significant positive relationship between right ventricular aneurysm and mortality after AMI has been demonstrated; further study is needed to clarify the relevant mechanisms.17 Epidemiological data indicate that females are affected by coronary artery disease approximately 10 years later than males.18


OBJeCTIVe Electrocardiographic (ECG) left atrial abnormality has been associated with stroke independently of atrial fibrillation (AF), suggesting that atrial thromboembolism may occur in the absence of AF. If true, we would expect an association with cryptogenic or cardioembolic stroke rather than non-cardio-embolic stroke.

MATeRIAl AnD MeTHODWe conducted a case-cohort analysis at Rohilkhand Medical College in Bareilly, a prospective cohort study of stroke risk factors. P-wave terminal force in lead V1 (PTFV1) was

manually measured from baseline ECGs of participants in sinus rhythm who subse-quently had ischemic stroke (N = 150) and a randomly selected sub cohort without stroke (N = 314) (Figure 1). Weighted Cox propor-tional hazards models were used to examine the association between PTFV1 and stroke etiological subtypes while adjusting for baseline demographic characteristics, history of AF, heart failure, diabetes, hypertension, tobacco use, and lipid levels.

ReSUlTS Participants with ischemic stroke had a significantly higher PTFV1 than those in

Table 1: Criteria for Left and Right Atrial Enlargement as Detected by CMR (cardiovascular magnetic resonance) vs ECG19

ECG Criteria Sensitivity (%) Specifi city (%) PPV (%) NPV (%)LAE Any ECG Criteria for LAE 90 21 31 84P > 0.11s 84 35 34 85P mitrale 8 99 86 74P axis < 30° 8 90 23 71NPTF-V1 > 0.04s·mm 37 88 47 76PPTF-aVL > 0.5 mm 44 60 30 73RAE Any ECG Criteria for R AE 17 96 33 91Inferior P waves > 2.5 mm 7 100 67 90Positive P wave in V1 > 1.5 mm 10 96 25 90CMR: Cardiovascular magnetic resonance. ECG: Electrocardiography. PPV: Positive predictive value. NPV: Negative predictive value. LAE: Left atrial enlargement. RAE: Right atrial enlargement. P mitrale: Notched P wave with interpeak duration > 0.04s. NPTF-V1 > 0.04s·mm: Area of negative P terminal force in lead V1 > 0.04s·mm. PPTF-aVL: Positive P terminal force in lead aVL. Inferior P waves: P wave in any of the leads II, III, or aVF.

Fig. 1: Association between PTFV1 and stroke in cases and sub cohort


the sub cohort (N=100 in ischemic stroke): (N=86 in cohort) as shown in Table 1. In an unadjusted model, PTFV1 was associated with a higher risk of ischemic stroke. This association did not substantially change after inclusion of potentially confounding or mediating covariates including a history of AF. Associations between PTFV1 and stroke were unchanged or stronger when we entirely excluded participants who had a baseline history of AF or were diagnosed with AF during follow-up. For cardioembolic or cryptogenic stroke, PTFV1 was associated with a 52% increase in risk. Among the 74% of participants with available baseline echocardiography data, the inclusion of left atrial size in our models attenuated the relationship between PTFV1 and all categories of stroke except cryptogenic stroke, although this association remained statistically nonsignificant. Further adjusting for left ventricular hypertrophy in the subgroup of participants with echocardiograms available at baseline did not materially change the results.

COnClUSIOnIn conclusion, the value of PTFV1 in predicting ischemic stroke documented by this study conducted in middle-aged hypertensive patients with ECG-LVH needs to be confirmed in larger studies representative of unselected hypertensive population.

RefeRenCeS1. Alwan A et al. Monitoring and surveillance of chronic

noncommunicable diseases: progress and capacity in high-burden countries. The Lancet 2010; 376:1861–1868.

2. The global burden of disease: 2004 update. Geneva, World Health Organization, 2008.

3. Comparative quantification of health risks: Global and regional burden of disease attributable to selected major risk factors. Geneva, World Health Organization, 2004.

4. Kannel WB. Blood pressure as a cardiovascular risk factor. JAMA 1996; 275:1571–1576.

5. Klag MJ, Whelton PK, Randall BL, Neaton JD, Brancati FL, Ford CE, et al. Blood pressure and end-stage renal disease in men. N Engl J Med 1996; 334:13–18.

6. Braam B, Taler SJ, Rahman M, et al. Recognition and management of resistant hypertension. Clin J Am Soc Nephrol 2017; 12:524–535.

7. Egan BM, Zhao Y, Axon RN, et al. Uncontrolled and apparent treatment resistant hypertension in the United States, 1988 to 2008. Circulation 2011; 124:1046–1058.

8. Daugherty SL, Powers JD, Magid DJ, et al. Incidence and prognosis of resistant hypertension in hypertensive patients. Circulation 2012; 125:1635–1642.

9. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke 1991; 22: 983–988.

10. Pisters R, Lane DA, Marin F, Camm AJ, Lip G Y. Stroke and thromboembolism in atrial fibrillation. Circ J 2012; 76:2289–2304.

11. Gage BF, et al. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001; 285:2864–2870.

12. Psaty BM, Manolio TA, Kuller LH, Kronmal, RA, Cushman M, Fried LP, et al. Incidence of and risk factors for atrial fibrillation in older adults. Circulation 1997; 96:2455–2461.

13. Vaziri SM, Larson MG, Benjamin EJ, Levy D. Echocardiographic predictors of nonrheumatic atrial fibrillation. The Framingham Heart Study. Circulation. 1994; 89:724–730.

14. Tsang TS, Barnes ME, Bailey KR, Leibson CL, Montgomery SC, Takemoto Y, et al. Left atrial volume: important risk marker of incident atrial fibrillation in 1655 older men and women. Mayo Clin Proc 2001; 76:467–475.

15. Morris JJ, Estes EH, Whalen RE, Thompson HK, McIntosh HD. P-wave analysis in valvular heart disease. Circulation 1964; 29:242–252.

16. Pohjola S, Siltanen P, Romo M. The prognostic value of the P wave morphology in the discharge ECG in a 5-year follow-up study after myocardial infarction. Am Heart J 1979; 98:32–38.

17. Siltanen P, Pohjola-Sintonen S, Haapakoski J, Mäkijärvi M, Pajari R. The mortality predictive power of discharge electrocardiogram after first acute myocardial infarction. Am Heart J 1985; 109:1231–1237.

18. Perkiomaki JS, Zareba W, Greenberg HM, Moss AJ. Usefulness of standard electrocardiographic parameters for predicting cardiac events after acute myocardial infarction during modern treatment era. Am J Cardiol 2002; 90:205–209.

19. Tsao, Connie W et al. “Accuracy of electrocardiographic criteria for atrial enlargement: validation with cardiovascular magnetic resonance” Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance vol. 10,1 7. 25 Jan. 2008, doi:10.1186/1532-429X-10-7


1Head of Department, 2Post-Graduate Student, JLNMCH, Bhagalpur, Bihar

Obstructive Sleep Apnea and Hypertension: A Reciprocal Menace

DP Singh1, Abhishek Kumar Tiwari2

REVIEW ARTICLE

InTRODUCTIOn: THe SYneRGY Of CAUSATIOnObstructive sleep apnea (OSA) with its complex web of association, is synergisti-cally conjugated with hypertension. The inadvertent physiological environment of sympathetic activation, oxidative stress, endothelial dysfunction and inflammation which is generated by the apneic episodes at night promote both nocturnal and daytime hypertension.

THe BlOCKAGe Of GATeWAY TO SOUnD SleeP OSA is defined by periods of partial or complete upper airway collapse leading to a disintegrated sleep pattern characterized by frequent awakenings and unwarranted day time sleepiness. In the presence of active ventilatory effort there is an absence of airflow for at least 10 seconds, this in turn is associated with fall of more than 4% in the saturation of oxygen (Figure 1). The rate at which the obstructive events occur per hour of sleep are identified as apnea hypopnea index (AHI) or respiratory disturbance index (RDI). AHI is the most commonly used

metric to determine the austerity of the OSA. Arbitrarily annotated threshold of AHI for defining OSA is 5 or more and when it is more than 30, OHA is considered to be severe. In the milieu of cardiovascular disease and risk assessment1,2 low AHI thresholds are equable because clinically significant cardiovascular outcomes are associated with an AHI as low as 5 events/hour3 or sometimes even lesser than that.

THe HeATHY DIPPhysiologically healthy individual show a 10-15% “Dip” in systolic and diastolic blood pressure during sleep.4 NREM sleep is characterized by parasympathetic system overpowering the sympathetic system leading to diminution of all the parameters of cardio-vascular activity, like, Blood pressure, heart rate and peripheral vascular resistance. This cozy relaxation period is punctuated during the REM sleep leading to a ephemeral surge in the heart rate, vascular resistance, pressure of the vessels and the overall sympathetic nerve activity. Fortunately this jerky REM constitutes only a fraction of the total period of sleep, the resultant measurement still favors a reduction of activity from the awake status. This sleep related relaxations are indis-pensible for the vascular health to an extent


that, any fallacy or reduction of the same can turn out to be and independent dictator of the cardiovascular system. A study by Eamon Dolan, et al. concluded that an increased night time systolic blood pressure can be an independent risk factor for the cardiovascular events5. The reinforcement of ABPM by the latest ACC/AHA and ESC guidelines is also backed by the fact that night time fluctuations in pressure have a long lasting effect on the cardiovascular system.

THe JeRKY RIDe ACROSS THe nIGHTObstructive apneas during sleep leads to hypercapnea and hypoxia both synergistically leading to sympathetic nerve stimulation by the activation of central and peripheral chemoreceptors respectively.6 Resumption of the respiration is marked by a rapid rise in heart rate along with a rise in blood pressure by the hypoxia induced vasoconstriction. Mean increase in blood pressure after an episode of sleep apnea has been found to be 32mmhg during NREM and 40 mmhg during REM.7 Ready to do the further damage is the state of arousal that follows the state of apnea which even in normal states is associated with instantaneous increase in cardiac sympathetic activity.

A HIT AND RUN OVER THE SYMPATHETIC SYSTEMThe microneurographic measurement of the muscle sympathetic neural activity has been shown to be continuously elevated during the day following the event of Obstructive sleep apnea.8 The catecholamines also found to maintain a surged states (Figure 1). The position of sleep arousals in the fabrication of hypertensive vascular environment was studied in canine models by creating artificial obstructive apneas during sleep. When comparing cyclically apnea induced awakening from sleep with auditory induced arousals devoid of respiratory disturbance, night-time mean BP augmented during both conditions, but only the apneas led to an increase in daytime BP (~16 mmHg). This implies that the alliance between OSA and hypertension is specific to the apnea-arousal bondages and cannot be decoded by increased arousals alone.9

ROle Of DICTATeD RAAS AnD TOXIC ReACTIVe OXYGen SPeCIeSHypoxia induced generation of the volatile reactive oxygen species along with a fall in the level of nitric oxide also contributes to the development of hypertension. Studies

Wakefulness

Sleep

Airway PatencyCompensation

HyperventilationCO2 / O2

Arousal/SleepFragmentation

POSTAPNEA

AirwayCollapse & Snoring

APNEAIncreased E�ort

Hypoxia/HypercapniaSympathetic Activation withadrenaline & cortisol release

DecreasedCompensation

PATHOLOGIC BREATHING CYCLE OSA

Fig. 1: Pathologic Breathing Cycle28


have demonstrated an increased level of superoxides in the neutrophils.10 A dysfunc-tional NO release leads to an inadvertent vasoconstriction,deteriorating the vascular tone.Dictated activation of RAAS also plays a role in development of hypertension in patients of OSA (Figure 2). Vasoconstrictor action of angiotensin II along with its ability to handle the sodium balance by the release of aldosterone can be an important mediator for the development of hypertension. In a study by Moller DS et al, Plasma angiotensin II and aldosterone were found to be high in OSA, and plasma angiotensin II was interrelated with BP. long-standing CPAP reduced BP, and this decline in BP was well in communication with the fall in plasma renin and angiotensin II levels.11

An InflAMMATORY STATe?The intermittent hypoxia induced altered oxygen saturation status cannot avoid the development of inflammation which in turn is linked with the fabrication of atheroscle-rosis and high vascular resistance levels. This

fact however is clouded by the presence of confounding factors like obesity. However, a study recently discussed that severity of OSA is self-governing predictor of IL 6 and CRP levels but interacts with obesity such that this web of association is established only in obese OSA patients. The validation for augmented levels of the pro-inflammatory cytokine TNF-α, on the other hand, is far more persuasive. Quite a lot of case-control studies have confirmed elevated TNF-α in patient with OSA, independent of obesity.12

An ARROW fACInG BOTH THe HeADSThe prevalence of hypertension in patients of OSA and vice-versa has led to the birth of an interest in search of the direction of causation. OSA in hypertension as such is not synonymous to hypertension in OSA. The frequency of hypertension in OSA patients is projected to be 30 - 70%.13 These prevalence is highly severity dependent, in those with severe OSA, the prevalence of hypertension was found to be higher (53%) as compared to

interleukin-6 are increased in OSAS patients, CPAP attenuates thedegree of increase of these parameters.12

OSAS patients have frequent awakenings at night and show elevatedsympathetic nervous activity. As the pulmonary stretch receptor reflex,which suppresses sympathetic nervous activation, is decreased inOSAS, the balance of the autonomic nervous activity shows a tendencytoward increased activity of the sympathetic nervous system.13 At thetime of the nocturnal episodes of hypoxia, in particular, a burst ofsympathetic nervous activity occurs, resulting in elevation of BP andheart rate. It is also widely recognized that apneic episodes in OSASpatients are exacerbated during rapid eye movement sleep, duringwhich sympathetic nervous activity is increased. Increased sympa-thetic nervous activity may also cause coronary spasm and inducevasospastic angina pectoris. Furthermore, periodic negative intrathor-acic pressure (�80mmHg, at most), together with a midnight surgeof BP, exerts mechanical stress on the ventricular and atrial walls,resulting in the development of left ventricular hypertrophy and leftatrial remodeling and, consequently, an elevated risk of heart failureand atrial fibrillation.13 The incidence of eccentric cardiomegaly hasbeen reported to be elevated in OSAS patients with left ventricularanomaly.14

A number of reports have shown that OSAS patients showdecreased serum levels of adiponectin because of increased sympa-thetic nervous activity,15 insulin resistance,16 activity of the renin–angiotensin–aldosterone (RAA) system17 and production of vasopres-sor hormones, and these changes are involved in the elevation of BPin OSAS patients. Plasma levels of endothelin-1 during the nightin OSAS patients are increased in relation to BP and the severityof OSAS.18

MEDICAL CARE PROCESS OF HYPERTENSION TAKING INTOCONSIDERATION OSASThe clinical signs from which OSAS can be suspected are shown inTable 1.1 It is a matter of course that typically obese patients with

hypertension who show symptoms such as daytime sleepiness,decreased concentration, depression and snoring at night should besuspected of having OSAS, but it is often the case that patients withhypertension do not have any subjective symptoms. It is thereforeimportant to suspect OSAS and obtain a detailed history, even in theabsence of subjective symptoms.Portable pulse oximetry is useful for screening OSAS; however,

accurate diagnosis and evaluation of OSAS severity can only be madeby polysomnography. The severity of OSAS is classified on the basis ofthe apnea–hypopnea index (number of apneic/hypopneic episodes perhour): 5–15, mild; 15–30, moderate; 30 or more, severe.The medical care process of masked hypertension, after taking

OSAS into consideration, is shown in Figure 2. First, BP levels inthe early morning are measured with a self-measured home BPmonitoring. When the level is 135/85mmHg or higher, the conditionis regarded as morning hypertension and treated by an antihyper-tensive drug with the goal of obtaining normal morning BP levels

Endothelial dysfunction

Nitric oxide

Oxidative stress

RAA system

Endothelin

Obstructive sleep apnea

Hypoxia(periodic)

Hypercapnea(periodic)

Pulmonary stretchreceptor stimulation

MicroarousalChemoreceptorstimulation

Sympatheticnerve activity

Hypertension

Non-dipper /Riser

pattern

Inflammation

Insulin resistance

Hypertensive targert organ damage

Negativeintrathoracicpressure

Baroreceptor sensitivity

Silent cerebral infarctsWhite matter disease

MicroalbuminuriaHypertensive heartdisease

LV hypertrophyDiastolic function

Left atrial enlargement

Silent cerebral disease

Figure 1 Mechanism of hypertension and target organ damage in obstructive sleep apnea syndrome. RAA, renin–angiotensin–aldosterone; LV, left ventricular.

Table 1 Key words detecting obstructive sleep apnea syndrome

Symptom Daytime sleepiness, reduced concentration, depression,

Indefinite complains (headache, malaise) at awakening or in

the morning, marked snoring, frequent awakening during the

night, nocturia, nocturnal dyspnea (feeling of suffocation)

Physical findings Obesity, micrognathia

Findings on

examination

Resistant morning hypertension including nocturnal hyper-

tension, Left ventricular hypertrophy (particularly when the

clinic and home BPs are normal), sleep-onset cardiovascular

events (including arterial fibrillation and ventricular arrhythmia),

metabolic syndrome

Abbreviation: BP, blood pressure.

Obstructive sleep apnea syndrome and hypertensionK Kario

538

Hypertension Research

Fig. 2: Pathophysiology of OSA24 [Adapted from- Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control. Kazuomi karuo. Hypertension Research volume32, pages537–541 (2009)]


those with moderate OSA (46%).13 The other way around, the prevalence obstructive sleep apneas in people with high blood pressure is found to be around 30-50% which, by all means can be considered to be an underes-timated data because of millions of missing cases pertaining to underdiagnosis.14 OSA has been listed as one of the most important common cause of secondary hypertension in the joint national committee guidelines. The resistant hypertension has an even more ardent affection for obstructive sleep apneas. The prevalence turns out to be whooping 83% if we consider only resistant hypertension.15A temporal causal relation between the two has been backed by a noteworthy longitudinal, prospective cohort study, the Wisconsin Sleep Cohort Study (WSCS) which established a statistically significant association. The WSCS established a dose response relationship with the increasing severity of obstructive sleep apnea and hypertension which was devoid of confounding risk factors like BMI, age, sex and the previous blood pressure.16 There has been no direct study to investigating the reign of OSA in the sphere of hypertension in Bhagalpur. We performed a retrospective cohort study in the patients admitted in the intensive care units of Jawaharlal Nehru Medical college, over a period of one year, total of 96 patients were diagnosed with OSA based on polysomnographic studies. When evaluate further, 49 patients (52%) patients were found to be having hypertension. Out of which 12 patients were having resistant hypertension. These results were consistent with the fact that there is a strong commu-

nication between these two entities and also that patients having resistant hypertension should be put under scanner for OSA as well.A retrospective study of patients with OSA diagnosed with polysomnography in Jawaharlal Nehru Medical College Bhagalpur, revealed that 46% of the patients had associated hypertension

DIPPeRS AnD THe RISeRSPopulation based studies putting into use the 24 h ambulatory BP monitoring (ABPM) have verified that those with a plunge in BP of <10% during the night (non-dippers) and those who accumulate an increase in blood pressure at night (risers) reveal a greater extent of end organ damage, risk of stroke, heart failure incidence, and increased jeopardy of renal disease evolution as compared to those hypertensives with conserved dipping, that is, a nocturnal decrease in BP of >10%.17

OSA In PeRTInACIOUS, ReSISTAnT HYPeRTenSIOnObstructive sleep apnea (OSA) is found even more in conjugation with patients with obstinate, resistant hypertension (Figure 3). In a prospective study on 41 patients with Resistant hypertension, 83% were diagnosed with OSA. These outcomes were cemented by Pratt-Ubunama et al, wherein the preva-lence of OSA was determined to be 85% in a study involving 71 patients with Resistant hypertension. Increasing severity of OSA is also found to be coupled with intricacy in controlling hypertension. As a corollary, in an observational study on patients with Resistant hypertension and OSA, treatment of OSA with continuous positive airway pressure facilitated de-escalation of antihypertensive drug therapy (either by dose reduction or discontinuation of ≥1 drugs) in 71% of the study patients.

COROllARY: PATIenTS TAKInG MORe THAn 3 AnTIHYPeRTenSIVeS SHOUlD Be SCReeneD fOR OSATreatment of OSA with the use of positive

Fig. 3: Diseases associated with OSA27


airway pressure has been used in the Resistant hypertensive patients. The HIPARCO study (Hipertension Arterial Refractaria Control on CPAP) reported by Martinez-Garcia et al illustrated a reduction in 24-hour mean and diastolic BP after 12 weeks of positive airway pressure.

CPAP:An UnReCOGnIZeD AnTIHYPeRTenSIVeMore than a few studies conclude that treating the sleep apnea with CPAP lowers the blood pressure and this has been duly validated by several randomized control trials. Almost all (but not all) studies displayed a BP lowering affect when controlled against sham devices or placebo, better effect being displayed with progressively improved compliance.18 Further studies were performed to clear up the clutter around this. An Indian, 3- month Sham CPAP – CPAP crossover study noticed a fall by 3.9/2.5 during CPAP as against the Sham CPAP.19

The Zaragoza Sleep Cohort Study instituted appreciably lower risk of hypertension after 12.2 years of follow-up between amenable CPAP users as against nonusers.20

IS THeRe AnY BOSS AMOnGST AnTIHYPeRTenSIVeS?There is an absence of any pinpointing guidelines pertaining to the class of antihy-pertensive medications to be used in treating hypertension in OSA patients. Supposedly, however, driven by the pathological mecha-nisms of arterial hypertension in OSA, drugs that modify RAAS and sympathetic system such as β-blockers and aldosterone antago-nists may be the best treatment options for such patients. The aldosterone antagonist such as spironolactone has been very effectual in diminishing the severity of OSA, especially in those with resistant hypertension. ACE inhibitors, angiotensin receptor blockers, and aldosterone antagonists have a moderate antihypertensive effect in moderate OSA. A study by Kraiczi et al, made it clear that B-blockers (atenolol) significantly reduced nocturnal diastolic and systolic BP more

effectively compared to calcium channel blockers, ACE inhibitors, and angiotensin receptor blockers.21 Diuretics, for the most part spironolactone, have been revealed to be the most convincing medication that relieves pharyngeal edema and secondary upper airway destabilization, hence healing both OSA severity and hypertension.22 Complicating this are some incriminating controversies, there has been some substantiations advising against the use of ACE inhibitors, because of the high frequency of drug induced dry cough along with increased upper airway inflam-mation and use of β-blockers which has been notorious for causing an unwelcomed weight gain which can aggravate OSA too. 22

MODIfICATIOnS fOR BReATHInG lIfe TO “lIfe”Lifestyle changes ought to be calculated as an integral part in the management of all patients with OSAS, including hypertensive OSAS. Patients with mild OSA can be bombarded with lifestyle modifications at the outset. Patients with milder OSA should be instructed to stay away from sleeping in the supine position, polysomnographic recordings have revealed this posture to be a breeding ground for OSA. Reducing the extra kilograms clearly relieves the lungs as they get the clearer airways to inspire. In an observational study, a weight loss of 10% predicted a 26% (95% CI 18–34%) fall in AHI25. Indirect evidence on the relationship between exercise and OSA comes from the Wisconsin sleep cohort study, which showed that lack of exercise was associated with increased severity of sleep-disordered breathing even after adjustment for BMI26. Giebelhaus et al. evaluated the impact of a 6-month structured exercise programme on OSA severity in a small group of OSA patients who were being treated concur-rently with CPAP and demonstrated a reduction in AHI off CPAP compared to pre-therapy.

DefIneD COHeRenCe WITH UnAnSWeReD QUeSTIOnSDespite of its wide prevalence and adverse clinical sequel, OSA in conjugation with hyper-tension still remains a relatively unexplored field which seeks a timely attention to avoid


discomfiture of irreparable wreckage. Hence, this field of interest needs even more keen observation with standardized, reproducible studies to validate the use of any particular antihypertensive and turning down the other. Without any visible doubts there is coherence between the OSA and vascular health and this needs to be properly exploited to mock down one, and by default the other cardiovascular enigma. Even outwardly healthy patients with OSA, devoid of any evidence for explicit cardio-vascular disease, have subtle but noteworthy abnormalities in vascular regulation at numerous levels, including the neural, humoral and endothelial levels. These fallacies may act to overcome even redundant vasoprotective mechanisms, hence predisposing to the potential evolution of clinically momentous functional and structural vascular alterations that may present as hypertension and/or stroke. Effective treatment of OSA helps bring a fall in blood pressure in hypertensive patients and may cut down nocturnal blood pressure in normotensive patients. These improvements may themselves have considerable favorable epidemiologic implications.

RefeRenCeS1. Somers VK, White DP, Amin R, et al: Sleep apnea and

cardiovascular disease: An American Heart Association/American College of Cardiology Foundation Scientific Statement from the American Heart Association Council for High Blood Pressure Research Professional Education Committee, Council on Clinical Cardiology, Stroke Council, and Council on Cardiovascular Nursing. Incollaboration with the National Heart, Lung, and Blood Institute National Center on Sleep Disorders Research (National Institutes of Health). Circulation 2008; 118:1080.

2. Bradley TD, Floras JS: Obstructive sleep apnoea and its cardiovascular consequences. Lancet 2009; 373:82.

3. Verrier RL, Josephson ME: Impact of sleep on arrhythmogenesis. Circ Arrhythmia Electrophysiol 2009; 2:450.

4. Autonomic activity during human sleep as a function of time and sleep stage.

Trinder J, Kleiman J, Carrington M, Smith S, Breen S, Tan N, Kim Y J Sleep Res 2001; 10:253-64.

5. Dolan E, Stanton AV, Thom S, et al. Ambulatory blood pressure monitoring predicts cardiovascular events in treated hypertensive patients – an Anglo-Scandinavian cardiac outcomes trial substudy. J Hypertens 2009; 27:876–885.

6. Berthon-Jones M, Sullivan CE. Ventilation and arousal

responses to hypercapnia in normal sleeping humans. J Appl Physiol 1984; 57:59–67.

7. Okabe S, Hida W, Kikuchi Y, et al. Role of hypoxia on increased blood pressure in patients with obstructive sleep apnoea. Thorax 1995; 50:28–34.

8. Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995; 96:1897–1904.

9. Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA. Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model. J Clin Invest 1997; 99:106–109.

10. Schulz R, Mahmoudi S, Hattar K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med 2000; 162:566–570.

11. Moller DS, Lind P, Strunge B, Pedersen EB. Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea. Am J Hypertens 2003; 16:274–280.

12. Pou KM, Massaro JM, Hoffmann U, et al. Visceral and subcutaneous adipose tissue volumes are cross-sectionally related to markers of inflammation and oxidative stress: the Framingham Heart Study. Circulation 2007; 116:1234–41.

13. Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study. Lavie P, Herer P, Hoffstein VBMJ 2000; 320:479-82.

14. Undiagnosed sleep apnea in patients with essential hypertension.

Fletcher EC, DeBehnke RD, Lovoi MS, Gorin AB Ann Intern Med. 1985; 103:190-5.

15. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension.

Logan AG, Perlikowski SM, Mente A, Tisler A, Tkacova R, Niroumand M, Leung RS, Bradley TD J Hypertens 2001; 19:2271-7.

16. Prospective study of the association between sleep-disordered breathing and hypertension. Peppard PE, Young T, Palta M, Skatrud J N Engl J Med 2000; 342:1378-84.

17. Associations between nondipping of nocturnal blood pressure decrease and cardiovascular target organ damage in strictly selected community-dwelling normotensives.Hoshide S, Kario K, Hoshide Y, Umeda Y, Hashimoto T, Kunii O, Ojima T, Shimada K Am J Hypertens 2003; 16:434-8.

18. Parati G, Lombardi C, Hedner J, Bonsignore MR, Grote L, Tkacova R, Levy P, Riha R, Bassetti C, Narkiewicz K, Mancia G, McNicholas WT, European Respiratory Society., EU COST ACTION B26 members. J Hypertens 2012; 30:633-46.

19. CPAP for the metabolic syndrome in patients with obstructive sleep apnea.

Sharma SK, Agrawal S, Damodaran D, Sreenivas V,


Kadhiravan T, Lakshmy R, Jagia P, Kumar A N Engl J Med 2011; 365:2277-86.

20. Association between treated and untreated obstructive sleep apnea and risk of hypertension. Marin JM, Agusti A, Villar I, Forner M, Nieto D, Carrizo SJ, Barbé F, Vicente E, Wei Y, Nieto FJ, Jelic S JAMA 2012; 307:2169-76.

21. Comparison of atenolol, amlodipine, enalapril, hydrochlorothiazide, and losartan for antihypertensive treatment in patients with obstructive sleep apnea.

Kraiczi H, Hedner J, Peker Y, Grote L Am J Respir Crit Care Med 2000; 161:1423-8.

22. Diuretics in obstructive sleep apnea with diastolic heart failure. Bucca CB, Brussino L, Batt isti A, Mutani R, Rolla G, Mangiardi L, Cicolin A Chest 2007; 132:440-6.

23. Cicolin A, Mangiardi L, Mutani R, Bucca C Mayo Clin Proc 2006; 81:53-5.

24. IMAGE CREDIT- Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control. Kazuomi karuo. Hypertension Research 2009; 32:537–541.

25. Peppard PE, Young T, Palta M, et al. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000; 284:3015–3021.

26. Peppard PE, Young T. Exercise and sleep-disordered breathing: an association independent of body habitus. Sleep 2004; 27: 480–484.

27. htt ps://mysleepsurvey.com/index.php?/treatment_must28. Leung and Bradely, “Sleep Apnea and Cardiovascular

Disease.” American Journal of Respiratory and Critical Care Medicine 164:2147–2165

Prevalence of Hypertension and co-morbidities in Young Diabetics in IndiaU Ayyagari1, B TS2, V S2, D CS3, J Gopal2, A Behl4, KG Seshadri1

ABSTRACTBackground and Aims: Prevalence of diabetes (DM) and associated co-morbidities are increasing in the young in India. The analysis was aimed to evaluate the comorbidities associated with young diabetes patients. Materials and methods: We undertook a retrospective data analysis for the prevalence of hypertension (HTN; newly diagnosed BP >140/90 or on medication for HTN) in young diabetics in Apollo Sugar Clinics across India (January 2016-June 2017; N=270000; verifiable lab results in n=13000). Results: Data is presented as percent (%) or mean (median), 1315 diabetics (10.1%) were <40 years old. HTN was present in 635 (48.3%). Of these: T2DM 613 (96.5%), T1DM 17 (2.7%), GDM 5 (0.8%). Mean age 35.8 (37); male 68.4%, female 31.6%; BMI 27.9 (27); HbAlc 8.3% (8.0); FPG 175.2 (156) mg/dL; PPG 267.9 (245) mg/dl; Serum Creatinine 0.87 (0.8) mg/dL; Urine microal-bumin 180.4 (15.3) mcg/mg; Lipid profile total cholesterol 194.8 (196.5) mg/dL, LDL 117.8 (121) mg/dL; HDL 39.8 (37) mg/dL; triglycerides 217.6 (221) mg/dL. Conclusion: Cardiovascular (CV) disease is a rising cause of mortality due to DM in India. Our data suggests 10% of our diabetics are age ≤40, with diagnosed HTN in 48% of this population. Presence of CV risk factors (dyslipidemia, obesity, metabolic syndrome) in this poorly controlled group of hypertensive, young diabetics protends a tsunami of morbidity, healthcare expenditure, and mortality. Screening for diabetes and associated CV risk factors at a younger age with early, aggressive management is necessary in our ethnically high-risk community. Fig. 1: Associated Co-morbidities

1Apollo Sugar Clinics, Chennai, Tamil Nadu; 2Apollo Sugar Clinics, Apollo Hospital, Chennai, Tamil Nadu; 3Apollo Sugar Clinics, Apollo Hospital, Bangalore, Karnataka; 4Apollo Sugar Clinics, Apollo Hospital, Mysore, Karnataka

ABSTRACT




1Senior Resident, 2Assistant Professor, 3Professor and Head, 4Additional Professor, Dept. of Endocrinology, Govt. Medical College, Thiruvananthapuram

Biochemically Negative Pheochromocytoma - 2 case Reports

Nandini Prasad1, Abilash Nair2, Geena Susan George1, Jabbar PK3, C Jayakumari4

CASE REPORT

ABSTRACTBackground: Biochemically negative pheochromocytoma is a rare entity. Case Charecterestics: Here we present two patients who presented as adrenal incidentalomas,biochemical evaluation was negative for pheochromocytoma but histopa-thology positive for the same.Conclusion: Every patient with adrenal incidentaloma should be prepared like a case of pheochromocytoma before surgery eventhough biochemically negative, else may prove fatal.

BACKGROUnDPheochromocytoma is a tumour arising from adrenal chromaffin tissue. It accounts for 0.2-0.6% of hypertension cases in an out patient clinic. Biochemically negative pheochromo-cytoma is very rare. Here we present two cases which were negative biochemically but proven by histopathology.

CASe RePORT

Case 1A 53 year old female was referred to our department when she was accidentally detected to have adrenal mass while evalu-ating for appendicitis. She was detected to have BP of 220/110 three years back but was

on irregular treatment. There were episodes of palpitation which were not precipitated by drugs and she never had typical paroxysms of pheochromocytoma. There was no cushingoid features, weakness, polyuria, excessive hair growth. On examination her BP was 170/110 in both upper limbs and 188 systolic in lower limb. Systemic examination were normal.Investigations – Routine hemogram and biochemistry including serum electrolytes were normal. CT Abdomen (Figure 1) showed a soft tissue density in left adrenal gland of size 36mm×36mm×26mm. It was heterog-enous and showed post contrast enhancement (90HU) with significant wash out. PAC/PRA ratio was 6 ng/dl/ng/ml/hr (normal). 24 hour urine metanephrine, normetanephrine were 63.19 µg/24 hours and 455.8 µg/24 hours respectively which was normal. Serum Testosterone and DHEAS were normal.


She underwent left adrenalectomy after preop-erative preparation was done like in a case of pheochromocytoma with alpha blochers, beta blockers and salt in diet. Histopathology report came as pheochromocytoma

Case 2A 39 year old female presented with inciden-tally detected adrenal mass in USS while evaluating for menorrhagia. She had a history of systemic hypertension patient for the past three. MRI Abdomen showed a right adrenal tumour of size 3.5×3.3×3.3 cm homogenous on T2, hyperintense with hypointense rim and hypointense on T1. No signal loss was observed in oppose phase images. PAC/PRA ratio was normal. Urine metanephrine and normetanephrine were 146 µg/24hours and 135 µg/24hours respectively. She underwent right adrenalectomy. Histopathology was

Fig. 2: Histopathology showing zellbellen pattern of pheochromocytoma

Case 2

A 39 year old female presented with incidentally detected adrenal mass in USS while evaluating for menorrhagia. She had a history of systemic hypertension patient for the past three. MRI Abdomen showed a right adrenal tumour of size 3.5×3.3×3.3 cm homogenous on T2, hyperintense with hypointense rim and hypointense on T1. No signal loss was observed in oppose phase images. PAC/PRA ratio was normal. Urine metanephrine and normetanephrine were 146 µg/24hours and 135 µg/24hours respectively. She underwent right adrenalectomy. Histopathology was suggestive of Pheochromocytoma showing zellbellen pattern (Figure 2).

Figure 2:

CONCLUSION

A suspicion of Pheochromocytoma should always be kept in mind while evaluating adrenal incidentaloma despite being biochemically negative as in our cases.1 They should undergo a proper preoperative preparation to avoid adrenergic crisis during or after surgery.2

REFERENCES

1.Lenders JW, Pacak K, Walther MM, et al. Biochemical diagnosis of pheochromocytoma: which test is best? JAMA 2002; 287:1427-1434

2. Chen Y. Pheochromocytoma presenting with normal urinary catecholamines and metabolites: a case report. Formos J Endocrin Metab 2009; 1:33-37

suggestive of Pheochromocytoma showing zellbellen pattern (Figure 2).

COnClUSIOnA suspicion of Pheochromocytoma should always be kept in mind while evaluating adrenal incidentaloma despite being biochem-ically negative as in our cases.1 They should undergo a proper preoperative preparation to avoid adrenergic crisis during or after surgery.2

RefeRenCeS1. Lenders JW, Pacak K, Walther MM, et al. Biochemical

diagnosis of pheochromocytoma: which test is best? JAMA 2002; 287:1427-1434

2. Chen Y. Pheochromocytoma presenting with normal urinary catecholamines and metabolites: a case report. Formos J Endocrin Metab 2009; 1:33-37

Fig. 1: CECT abdomen showing soft tissue density in the left adrenal gland

BIOCHEMICALLY NEGATIVE PHEOCHROMOCYTOMA -2 CASE REPORTS

Dr. Abilash Nair1, Dr. Nandini Prasad2, Dr.Geena Susan George2, Dr. Jabbar P.K.3, Dr. C. Jayakumari4

Department of Endocrinology Government Medical College Thiruvananthapuram 1Assistant Professor, 2Sr. Resident, 3HOD, 4Additional Professor, Dept. of Endocrinology, Govt. Medical College, Thiruvananthapuram

Background

Pheochromocytoma is a tumour arising from adrenal chromaffin tissue .It accounts for 0.2-0.6% of hypertension cases in an out patient clinic. Biochemically negative pheochromocytoma is very rare. Here we present two cases which were negative biochemically but proven by histopathology.

CASE REPORT

Case 1

A 53 year old female was referred to our department when she was accidentally detected to have adrenal mass while evaluating for appendicitis. She was detected to have BP of 220/110 three years back but was on irregular treatment. There were episodes of palpitation which were not precipitated by drugs and she never had typical paroxysms of pheochromocytoma. There was no cushingoid features, weakness, polyuria, excessive hair growth. On examination her BP was 170/110 in both upper limbs and 188 systolic in lower limb. Systemic examination were normal.

Investigations – Routine hemogram and biochemistry including serum electrolytes were normal. CT Abdomen (Figure 1) showed a soft tissue density in left adrenal gland of size 36mm×36mm×26mm. It was heterogenous and showed post contrast enhancement (90HU) with significant wash out. PAC/PRA ratio was 6 ng/dl/ng/ml/hr (normal). 24 hour urine metanephrine, normetanephrine were 63.19 µg/24 hours and 455.8 µg/24 hours respectively which was normal. Serum Testosterone and DHEAS were normal.

She underwent left adrenalectomy after preoperative preparation was done like in a case of pheochromocytoma with alpha blochers, beta blockers and salt in diet. Histopathology report came as pheochromocytoma

Figure 1:


1Resident, 2Professor, Department of General Medicine, 3Associate Professor, Department of Endocrinology, Father Muller Medical College, Father Muller Road, Mangaluru, Karnataka 575002

The Immediately Evident may be Insufficient

Vishnumoorthy1, Smitha Bhat2, Sudeep K3

CASE REPORT

ABSTRACTWe report the case of a 72 year old gentleman, a known hypertensive, who presented with giddiness, vomiting and reduced responsiveness. O/E: hemodynamically stable, conscious but drowsy, no focal neurological deficit. Labs revealed serum Na:112mEq/L, TSH was mildly elevated at 6.5. Thiazides withheld, patient improved with 3% saline. Discharged with normal sodium, on Telmisartan and Thyroxine. 2 weeks later, patient presented with vomiting and headache. Labs revealed Na: 117mEq/L. In view of severe head ache, neuroimaging was done, revealing a pituitary macro adenoma with displaced stalk, no chiasmal compression. Prednisolone was added to the prescription in view of non-secretary adenoma.The neurosurgeon opined that surgery could be safely deferred for 6 months as per patient request.

InTRODUCTIOnHypertension is one of the common non communicable disease with the prevalence in India of 29.8%.1 and in world of 40%. Approximately 7.5 million, 12.8% of the total deaths is estimated to be due to elevated blood pressure.2 Treating Hypertension improves outcomes, however many antihypertensive have adverse effect, which must be kept in mind during the prescription and follow-up.

CASe RePORTWe report the case of 72 year old gentleman, a

known hypertensive, who was on hydrochlo-rothiazide 25mg daily as a antihypertensive, who presented with giddiness, vomiting, and reduced responsiveness. On examination he was hemodynamically stable and was conscious but drowsy. Systemic examination was essentially normal. There were no focal neurological deficits. Labs revealed a serum sodium of 112 mEq/L, and TSH was mildly elevated at 6.5. Thiazides were withheld suspecting thiazide induced hyponatremia and the patient improved after administration of 3% saline. He was discharged with normal sodium levels, telmisartan as antihypertensive and thyroxine.2 weeks later the patient presented once more with vomiting and headache. He was


The Immediately Evident may be Insufficient

Vishnumoorthy1, Smitha Bhat2, Sudeep K3

conscious, oriented with normal systemic examination. Labs revealed severe hypona-tremia with sodium of 117 mEq/L (investiga-tions of two visits summarised in Table 1). In view of the severe headache with vomiting, neuroimaging was planned and MRI brain was done which revealed a pituitary macro adenoma with displaced stalk and no chiasmal compression (Figure 1 and 2). Prednisolone was added to the prescription in view of the non- secretory adenoma. The neurosurgeon opined that surgery could safely be deferred for 6 months as per patient request.

DISCUSSIOnThe short term antihypertensive action of thiazides is by diuresis, whereas in the longterm, thiazides cause vascular smooth muscle relaxation.3 Thiazides increases water permeability and water reabsorption in inner medullary collecting duct. They also increase

sodium and potassium excretion, which might leads to hyponatremia and hypokalemia.4

Treatment of thiazide induced hyponatremia based on patient’s level of consciousness. If conscious, correction is done orally, if not then IV correction is done with 3% saline. Thiazides must be withheld.5

Pituitary adenoma causes hyponatremia by various mechanisms: hypothyroidism, ACTH deficiency, SIADH, cerebral salt wasting syndrome. Hypothyroidism causes increased ADH secretion - this will cause inability to excrete free water thus resulting in hyponatremia. It also decreases glomerular filtration rate which will also decreases free water excretion.6 ACTH deficiency causes secondary adrenal insufficiency which causes decreased cortisol secretion this will increase ADH secretion thus hyponatremia.7 In cerebral salt wasting syndrome hypona-tremia is by disruption of sympathetic neural input to the kidney and natriuresis induced by natriuretic peptides.8 Treatment is by hormone supplementation. Definitive cure is by surgery.

COnClUSIOnWe present this case to emphasize that a particular observation, In this case hypona-

vomiting, and reduced responsiveness. On examination he was hemodynamically stable and

was conscious but drowsy .Systemic examination was essentially normal. There were no

focal neurological deficits. Labs revealed a serum sodium of 112 mEq/L, and TSH was

mildly elevated at 6.5 . Thiazides were withheld suspecting thiazide induced hyponatremia

and the patient improved after administration of 3% saline. He was discharged with normal

sodium levels, telmisartan as antihypertensive and thyroxine.

2 weeks later the patient presented once more with vomiting and headache. He was

conscious, oriented with normal systemic examination. Labs revealed severe

hyponatremia with sodium of 117 mEq/L. In view of the severe headache with

vomiting, neuroimaging was planned and MRI brain was done which revealed a

pituitary macro adenoma with displaced stalk and no chiasmal compression.

Prednisolone was added to the prescription in view of the non- secretory adenoma.

The neurosurgeon opined that surgery could safely be deferred for 6 months as per

patient request.

Investigations:

1st visit 2nd visit

Blood pressure 130/80mmHg 120/80mmHg

Sodium 108mEq/L 117mEq/L

Potassium 3.75mEq/L 3.88mEq/L

TSH 6.54uIU/ml 4.89uIU/ml

FT4 0.610ng/dl 0.541ng/dl

Creatinine 1.16mg/dl 0.89mg/dl

MRI brain

FIGURE01:.T1W MRI CORONAL SECTION FIGURE02: T1W MRI SAGITAL SECTION

Transverse diameter of 13.5mm

vomiting, and reduced responsiveness. On examination he was hemodynamically stable and

was conscious but drowsy .Systemic examination was essentially normal. There were no

focal neurological deficits. Labs revealed a serum sodium of 112 mEq/L, and TSH was

mildly elevated at 6.5 . Thiazides were withheld suspecting thiazide induced hyponatremia

and the patient improved after administration of 3% saline. He was discharged with normal

sodium levels, telmisartan as antihypertensive and thyroxine.

2 weeks later the patient presented once more with vomiting and headache. He was

conscious, oriented with normal systemic examination. Labs revealed severe

hyponatremia with sodium of 117 mEq/L. In view of the severe headache with

vomiting, neuroimaging was planned and MRI brain was done which revealed a

pituitary macro adenoma with displaced stalk and no chiasmal compression.

Prednisolone was added to the prescription in view of the non- secretory adenoma.

The neurosurgeon opined that surgery could safely be deferred for 6 months as per

patient request.

Investigations:

1st visit 2nd visit

Blood pressure 130/80mmHg 120/80mmHg

Sodium 108mEq/L 117mEq/L

Potassium 3.75mEq/L 3.88mEq/L

TSH 6.54uIU/ml 4.89uIU/ml

FT4 0.610ng/dl 0.541ng/dl

Creatinine 1.16mg/dl 0.89mg/dl

MRI brain

FIGURE01:.T1W MRI CORONAL SECTION FIGURE02: T1W MRI SAGITAL SECTION

Transverse diameter of 13.5mm

Fig. 1: T1W MRI Coronal Section Fig. 1: T1W MRI Sagital Section

Table 1: Investigations of First and Second Visit1st visit 2nd visit

Blood pressure 130/80mmHg 120/80mmHgSodium 108mEq/L 117mEq/LPotassium 3.75mEq/L 3.88mEq/LTSH 6.54uIU/ml 4.89uIU/mlCreatinine 1.16mg/dl 0.89mg/dl


tremia might be multifocal in origin and one should not be satisfied with the obvious diagnosis. Additionally, the only mildly elevated TSH could have been a clue to the pituitary pathology, if FT4 had been ordered and interpreted at that point of time.

RefeRenCeS1. Anchala R, Kannuri NK, Pant H, Khan H, Franco

OH, Angelantonio E Di, et al. Hypertension in India: a systematic review and meta-analysis of prevalence, awareness, and control of hypertension. 2014;32(6).

2. Day WH. A global brief on Hyper tension World Health Day 2013. 2013;

3. Duarte JD, Cooper-DeHoff RM. Mechanisms for blood pressure lowering and metabolic effects of thiazide and thiazide-like diuretics. Expert review of

cardiovascular therapy 2010; 8:793-802. doi:10.1586/erc.10.27.

4. César KR, Magaldi a J. Thiazide induces water absorption in the inner medullary collecting duct of normal and Brattleboro rats. Am J Physiol 1999; 277:F756–60.

5. Hwang KS, Kim GH. Thiazide-induced hyponatremia. Electrolyte Blood Press 2010; 8:51–7.

6. Gynecol UO. Hyponatraemia , hypothyroidism , and role of arginine-vasopressin Medical Editors Trial Amnesty 1997; 350:11–2.

7. Report AC. Patient With Severe Hyponatremia Caused by Adrenal Insufficiency Due to Ectopic Posterior Pituitary Lobe and Miscommunication Between Hypothalamus and Pituitary. 2016; 95:1–6.

8. Abcar AC. Hyponatremia — What Is Cerebral Salt Wasting ? 2010; 14:62–5.

HYPERTENSION SOCIETY INDIASecretariat: Dr. B.R. Bansode, Room No.12, Bombay Mutual Terrace,

534, Sandhurst Bridge, Opera House, Mumbai 400 007.

Nominations are invited for the following positions on the Executive Committee for the year 2019-2020.

Vice President ................................................. One

Secretary General ........................................... One

Jt. Secretary .................................................... One

Members, Executive Committee ..................... Four

IMPORTANT:

1. For the post of Vice President, the member must have served on the Executive Committee for two terms of two years each of HSI in the past.

2. For the post of Secretary General, the member must have served on the Executive Committee for two terms of two years each of HSI in the past and must be from Head Quarters.

3. The nomination form duly proposed and seconded candidates must reach the Secretariat by 10th July, 2019.


28th national Conference on Hypertensionunder the auspices of Hypertension Society India

Date : 20th - 22nd September 2019 Venue : Hotel Trident, Nariman Point, Mumbai 400 021

ABSTRACT SUBMISSION FORM FOR FREE COMMUNICATIONSDEADLINE FOR RECEIPT OF ABSTRACTS : July 15th, 2019.

Name of Presenting Author ____________________________________________________________________________________(family name followed by initials)Co-Author(s) ___________________________________________________________________________________________________________

Institutions__________________________________________________________________________________________________Postal Address __________________________________________________________________________________________________________________________________________________________________________________________________________Tel .: ____________________________Fax : ___________________________E-mail : ___________________________________

INSTRUCTIONS

Abstracts must be related to original work and must confirm to acceptable ethical standards.

TYPING• Practicetypingtheabstractfirstonaseparatepieceofpaper.• Typingmustbeofhighquality.Ablackcarbontypewriterribbonoraletterqualityprintermustbeused.Usedoublespacing.• Simpletablesorgraphsmaybeincludedprovidedtheyfitwithintherectangularspaceandaretypedordrawninblackink.• Typeabstractwithinoutline–donotgooverthelines.• Avoiderasures.• TypeTITLEinCAPITALLETTERSinthetop–box.• TypeNAME(S)ofAUTHORS(S)precededbyINITIALSinCAPITALLETTERSomittingtitles,degrees,etc.inthesecondbox

withthenameofinstituteandcityinupperandlowercase.• Underline the name of the presenting author.• Useblackinktoaddsymbolsnotavailableonthetypewriterorprinter.

GENERALAll Presenting Authors Must Enroll for the Conference as Delegates• Abstractsmustbereceivedbythedate,15thJuly,2019.• Eachauthormaypresentonlyonefreecommunicationbutmaybeco-authorofadditionalabstracts.• Ifaccepted,yourabstractwillbereproducedexactlyasitistypedandwillappearintheJournalofH.S.I.,whichwillbedistributedtoallthe

members.• ThedecisionofScientificCommitteewillbefinalastowheretoaccommodatethepaper.• Approximatetimeallottedforeachpaperwillbe5minutesforpresentationand3minutesfordiscussiononit.• IfauthorsofacceptedpapersremainabsentwithoutpriorintimationtotheChairmanoftheSc.CommitteeofHSI,theirpapersmaynotbe

consideredfortwosubsequentconferences.• TheabstractshouldbeasinformativeaspossibletoincludeObjectofthestudy,Methodology,SummaryofresultsandConclusionreached.• [email protected] / [email protected]

For Conference Registration contact :

Prof. Siddharth N. ShahOrganizing Chairperson, HSICON 2019

BombayMutualTerrace,534,SandhurstBridge,Mumbai400007. Phones:022-23612146/23612578•e-mail:[email protected]


HYPERTENSION SOCIETY INDIAABSTRACT FORM

PROCESSING OF ABSTRACTS

Abstracts will be reviewed and rated by a national panel of referees prior to final determination on acceptance by the Scientific Programme Committee.

UNDERTAKING

I have read the above instructions and would abide by the decision of the Scientific Committee. I also say that the material presented is my original work and that I have not presented it before in any other Society or Hypertension Society of India.

Place: __________________

Date: ___________________ Submitting Author’s Signature




TO ALL LIFE MEMBERS OF THE SOCIETY

Nominations are invited for the following positions on the Executive Committee for the year 2019-2020.

Vice President .........................................One

Secretary General ...................................One

Jt. Secretary ............................................One

Members, Executive Committee .............Four

IMPORTANT:

1. For the post of Vice President, the member must have served on the Executive Committee for two terms of two years each of HSI in the past.

2. For the post of Secretary General, the member must have served on the Executive Committee for two terms of two years each of HSI in the past and must be from Head Quarters.

3. The nomination form duly proposed and seconded candidates must reach the Secretariat by 10th July, 2019.

TEAR HERE



NOMINATION FORM

I wish to apply for the post of _________________________________________on the Executive Committee and if elected, will abide all the rules and regulations in force.

Name of the Candidate ___________________________________________________________________________

Address of the Candidate _________________________________________________________________________

Tel. Nos. _______________________________________ e-mail __________________________________________

Name of the Proposer* ___________________________ Name of the Seconder* ____________________________

Address of the Proposer __________________________ Address of the Seconder ___________________________

______________________________________________ _______________________________________________

Signature of the Proposer _________________________ Signature of the Seconder __________________________

Date: _______________ Signature of the Candidate __________________________

*Proposer & Seconder should be a member of Hypertension Society of India


28th national Conference on Hypertensionunder the auspices of Hypertension Society India

Date : 20th - 22nd September 2019 Venue : Hotel Trident, Nariman Point, Mumbai 400 021.

Dr. P.J. MEHTA YOUNG SCIENTIST AWARD

As you are aware for the past many years we have been giving the Young Scientist Award for the Best

paper presentation at the National Conference of HSI.

Papers are invited from young research workers (below 35 years of age) who have done original

research work in the field of hypertension and related subjects. These papers will be judged by a panel

of referees. The finalists will be required to present their papers at the National Conference. From

these will be selected the recipient of the Dr. P.J. MEHTA YOUNG SCIENTIST AWARD. The research

worker who submits his paper must attach a certificate indicates his date of birth.

The finalists will be given 2nd Class A/c train fare to and from their hometown.

Please send 5 copies of the full manuscript of the paper along with the abstract typed in the abstract

form enclosed along with to Dr. B.R. Bansode, Room No. 12, Bombay Mutual Terrace, 534, Sandhurst Bridge, Opera House, Mumbai 400 007

LAST DATE OF RECEIPT OF MANUSCRIPT: 15th July, 2019.

Dr. B.R. Bansode, Secretary General, HSI


The Effect of Hypertension and Diabetes Mellitus on White Matter changes in MRI Brain: A comparative Study between Patients with Alzheimer’s Disease and an Age-matched control groupUma Sundar1, Abhilasha A Manwatkar2, Anagha R Joshi3, Prashant Bhandarkar4

ABSTRACTBackground: White matter hyperintensities (WMH) on MRI brain in the periventricular and deep white matter regions are commonly seen in older persons with normal cognition and in patients with AD.Aims: To compare presence and severity of WMHs in patients with AD with that in a cognitively normal control group, and to evaluate effect of presence of Hypertension and Diabetes on WMHs in both groups.Material and Methods: Thirty four patients with AD were serially recruited from Neurology and Psychiatry OPDs. An age and gender matched cohort of 24 persons with MMSE over 27/30 from the community acted as controls. Vascular risk factors, MMSE and MRI brain were assessed in all. Fezeka’s and Pasquier grading of WMH and atrophy were done. Periventricular WMHs (PVWMH) and Deep WMH (DWMH) were assessed separately.Results and Conclusions: Overall, Periventricular WMHs of grade 2 and over were seen in 19/34 patients, and in 7/24 controls (P value 0.044). Significantly higher grades of PVWMHs were seen in hypertensives as compared to non-hypertensives in the case group, and in women compared to men. In the control group, hypertension had no effect on severity of PVWMHs. Among both Diabetics and non-diabetics, no difference in PVWMHs was found between the case and control groups. DWMHs were, conversely, seen only in the control group.Overall, over a quarter of cognitively normal older persons had WM hyperintensities of grade 2 and over on MRI brain; 55% of AD patients had PVWMH of Gd 2 or over, and no DWMHs.

1Professor of Medicine Department, 2Assistant Professor, 3Professor of Radiology Department, 4Statistician, LTM Medical College and LTMG Hospital, Mumbai, Maharashtra

Retrospective Study to Evaluate Efficacy and Safety of Azilsartan in Diabetic Hypertensive Patients from Hospital in gujaratMA Agarwal1, D Agarwal1, DC Raval1, DU Petare2, DYS Petare2

ABSTRACTBackground and Aims: Management of Diabetic hypertensives is a challenge. With availability of newer sartan such as Azilsartan which is more potent for reducing blood pressure was explored in Tertiary care centre of GujaratMaterials and Methods: This retrospective audit was approved by institutional ethics committee. Data from hospital records in Medilink Hospital Research Centre of Ahmedabad collected and analyzed with appropriate statistical tests.Results: Total diabetic hypertensive patients data available was 201 as per inclusion & exclusion criteria. Mean age of population was 54.7 + 9.1 years & sex ration as 1.7:1 (M:F). Azilsartan was used as an add on to ongoing antihypertensive drugs in 90% patients & 10% were on Azilsartan monotherapy. Significant (p<0.05) reduction in mean SBP/DBP observed at 1st follow up visit (around 8th week: 8.6/7.3 mmHg) & 2nd follow up visit (around 12th week: 19.2/12 mmHg) as compared to basel,ine (Baseline Mean SBP/DBP: 156.1/97.3, 1st visit Mean SBP/DBP: 147.5/90, 2nd Visit Mean BP 136.9/85.3). Target BP of <140/90 was achieved by 42% patient on 2nd follow up visit. Serious adverse events/Death were not reported in records.

1Medilink Hospital Research Centre, Ahmedabad, Gujarat; 2Medical Services, Glenmark Pharmaceuticals, Mumbai, Maharashtra

ABSTRACTS


Pulmonary Hypertension in Patients with End Stage Renal Disease on Maintenance Hemodialysis-A cross-sectional StudyNarinder Pal Singh1, Arushi Nautiyal2, Ajay Karol3, Neeru P Aggarwal4, Gaurav Minocha5, Anish Kumar Gupta6

ABSTRACTBackground: Pulmonary Hypertension (PH) in End Stage Renal Disease (ESRD) on Maintenance Hemodialysis (HD) portends a poor outcome in patients undergoing dialysis. Methods: 50 patients with ESRD undergoing regular hemodialysis for at least 3 months were included. Biochemical parameters- hemoglobin, urea, creatinine, albumin, calcium, phosphorus and PTH assessed post dialysis. All patients underwent 2D echocardiography one hour after dialysis to avoid overestimation of pulmonary artery pressures. Measurement of various parameters was carried out including right atrial and ventricular dimensions, tricuspid annular plane systolic excursion, flow across tricuspid and pulmonary valves and tissue doppler imaging of the annular plane. PH was defined as mean right ventricular systolic pressure ≥25 mmHg. Variables were compared between two groups- subjects with PH and Non-PH.Results: Seventeen patients were detected to have PH. All baseline biochemical parameters did not show significant difference between two groups. On ECHO, right atrial and ventricular enlargement and pulmonary vascular resistance were significantly higher in PH group. LA vol index greater than 34ml/m2 was detected in 94.1% patients with PH as opposed to 51.5% in non PH. LVEDP was detected to be significantly higher in PH compared to Non PH (p=0.001; 94.1% vs 39.4%). Mean values of ejection fractions were also significantly different.Conclusion: This study suggests that up to one third of ESRD patients on HD develop PH. Echocardiography findings reveal a significant association between raised LVEDP and increased pulmonary artery pressures. Thus, volume overload and diastolic dysfunction (heart failure with preserved ejection fraction) appear to be the main contributors to devel-opment of PH.

1Senior Director, Internal Medicine, 2Resident, Medicine, 3Consultant, Department of Cardiology, 4Associate Director, Department of Nephrology, 5Principal Consultant, Department of Cardiology, 6Research Associate, Medicine, Max Super Speciality Hospital, Vaishali, Ghaziabad, Uttar Pradesh

A Randomized, Double-blinded, controlled, Multicentre Phase III Study to Evaluate the Efficacy and Safety of Telmisartan/Amlodipine/Hydrochlorothiazide compared to Telmisartan/Hydrochlorothiazide in Patients with Essential HypertensionJS Hiremath1, K Chokalingam2, G Mathan3, P Naveen Chander Reddy4, A Sharma5, S Dhawan6, A Toppo7

ABSTRACTObjective: Triple drug combination has shown to be effective in controlling blood pressure (BP) with low rates of drug-related side effects. The present study was conducted to compare the efficacy and safety of a triple pill of telmisartan/amlodipine/hydrochlorothiazide (HCTZ) with a dual combination of telmisartan/HCTZ in treating hypertensive patients who did not respond to monotherapies.Methods: A total of 512 patients were randomized to receive either low-dose triple pill or the dual combination therapy. The primary endpoint was BP normalization after 8 weeks. The secondary endpoints were BP normalization at 4 weeks, changes in BP from baseline to Week 8, comparison of BP normalization between treatment groups, and difference in BP responder rates. The analysis was conducted on the intent-to-treat (ITT), modified intent-to-treat (mITT) and per protocol (PP) population.Results: Statistically significant difference was noted between triple pill and telmi+HCTZ in the normalization of BP at Week 8 in the mITT (p=0.041) and PP (p=0. 038) populations. Also, a statistically significant improvement was observed in BP normalization in triple pill group compared with telmi+HCTZ group in ITT (p=0.022) and mITT (p=0.015) populations after 4 weeks. At Week 8, a significant reduction in BP was seen compared to the baseline in both the treatment groups. There was no statistically significant difference between the two treatment groups in BP normalization. Diastolic BP responder rates were significantly better for triple pill group in PP population (p=0.046). Conclusions: The triple pill was found to be effective in achieving early normalization of BP in hypertensive patients who did not respond to monotherapies.

1Senior Director, Internal Medicine, 2Resident, Medicine, 3Consultant, Department of Cardiology, 4Associate Director, Department of Nephrology, 5Principal Consultant, Department of Cardiology, 6Research Associate, Medicine, Max Super Speciality Hospital, Vaishali, Ghaziabad, Uttar Pradesh

28TH ANNUAL CONFERENCE OFHYPERTENSION SOCIETY OF INDIA

&1ST INTERNATIONAL KIDNEY AND

HYPERTENSION CONFERENCE

20-22 September 2019Hotel Trident, Nariman Point, Mumbai 400021

ABSTRACTS


28TH ANNUAL CONFERENCE OFHYPERTENSION SOCIETY OF INDIA

&1ST INTERNATIONAL KIDNEY AND

HYPERTENSION CONFERENCE

20-22 September 2019Hotel Trident, Nariman Point, Mumbai 400021


Invitation

It is with great pleasure we welcome you to the 28th Annual HSICON & 1st International Kidney & Hypertension Conference from 20th to 22nd September, 2019 at Hotel Trident, Nariman Point, Mumbai 400 021.

This conference will be targeting clinical aspects of treatment of kidney diseases in conjunction with hypertension a much neglected and a silent killer. Eminent International and National Faculty will share their expertise in the treatment of kidney & hypertension. The conference will also discuss Hypertension, Diabetes, Obesity and Lipids.

Physicians and Nephrologists will participate in this event from India & different parts of the world.

This three day mega event will have many case studies, uptodate diagnostics & bedside treatment solutions.

Workshop & interactive sessions will be the hallmark of this conference.

We look forward to welcome you at Mumbai.

With regards

Siddharth N. ShahORGANISING CHAIRMAN

Ashok KirpalaniPRESIDENT

PRESIDENTDr. Ashok Kirpalani

ORGANISING CHAIRMANDr. Siddharth N. Shah

SECRETARY GENERALDr. B. R. Bansode

ORGANISING COMMITTEE

TREASURERDr. A. M. Bhagwati

SCIENTIFIC COMMITTEE CHAIRMAN

Dr. Dilip Kirpalani

ORGANIZING SECRETARIESDr. Hardik ShahDr. R. B. Phatak

LAST DATE OF ABSTRACTS15TH AUGUST 2019


Invitation

It is with great pleasure we welcome you to the 28th Annual HSICON & 1st International Kidney & Hypertension Conference from 20th to 22nd September, 2019 at Hotel Trident, Nariman Point, Mumbai 400 021.

This conference will be targeting clinical aspects of treatment of kidney diseases in conjunction with hypertension a much neglected and a silent killer. Eminent International and National Faculty will share their expertise in the treatment of kidney & hypertension. The conference will also discuss Hypertension, Diabetes, Obesity and Lipids.

Physicians and Nephrologists will participate in this event from India & different parts of the world.

This three day mega event will have many case studies, uptodate diagnostics & bedside treatment solutions.

Workshop & interactive sessions will be the hallmark of this conference.

We look forward to welcome you at Mumbai.

With regards

Siddharth N. ShahORGANISING CHAIRMAN

Ashok KirpalaniPRESIDENT

PRESIDENTDr. Ashok Kirpalani

ORGANISING CHAIRMANDr. Siddharth N. Shah

SECRETARY GENERALDr. B. R. Bansode

ORGANISING COMMITTEE

TREASURERDr. A. M. Bhagwati

SCIENTIFIC COMMITTEE CHAIRMAN

Dr. Dilip Kirpalani

ORGANIZING SECRETARIESDr. Hardik ShahDr. R. B. Phatak

LAST DATE OF ABSTRACTS15TH AUGUST 2019

Registration FORM

HSI Life Membership No.:

Name (Use BLOCK Letters):

Surname First Name Middle Name

Sex: Male Female

Designation:

Department:

Name of Institution:

Qualifi cation / Degree:

Mailing Address:

Plot / House No. & Street:

City / Town / Village:

State: Pin:

Telephone: (Offi ce) (Resi.)

Mobile:

e-mail:

Accompanying Persons:

1.

Sex: Male Female Age

DEMAND DRAFT PAYABLE IN FAVOUR OF “HSICON 2019” PAYABLE AT MUMBAI.

Please fi nd enclosed D.D. of Rs. .................................................. No. ...................................................................Date .........................................................

Bank ...............................................................................................Branch ........................................................................................................................................

Appropriate Registration Fees in (`) INR

Non-Residential Till 30th June, 2019 Delegate (Members of HSI)

` 6,000

Delegate (Non Member of HSI)

` 8,000With Membership of HSI

Accompanying person ` 8,000

Post Graduate ` 4,000

Appropriate Registration Fees in (`) INR

Residential Package(2 Nights) + Registration

Till 30th June, 2019

Single Occupancy ` 40,000

Double Occupancy ` 50,000

Registration Details

Hypertensi

on Society ofIndia

SecretariatProf. Siddharth N. ShahOrganising Chairman

Bombay Mutual Terrace, 534, Sandhurst Bridge, Mumbai 400007Phones: 2361 2146 / 2361 2578 • Telefax: 022-2361 2578e-mail : [email protected] • Website : www.hsindia.org


Workshop on Measurement of Blood Pressure

Role of Sacubritil / Valsartan in Hypertension and Heart Failure

Aldosterone Antagonism / Pathway 2

Epidemiology Oration : Current Status of Hypertension and CKD in India

New Antihypertensives

Renal Denervation, Baroreflex Stimulation and Automonic Nervous System in Hypertension

Newer Devices and Strategies for BP Control

Hypertension in Pediatric Population

Keynote Address : Cost Effective Strategies for BP Control in India

Resistant Hypertension

Renovascular Hypertension and Role of CO2 Angiography of Renal Arteries

Concept of HI (Health Incubator) Lab and Speciality Hypertension Clinics

U N Mehta Oration

P J Mehta Young Investigator Award

Dr. Atul Pathak, France

Dr. Gregory Hundemer, Canada

Dr. George Thomas, USA

Dr. Hemant Kulkarni, Australia

Dr. Mohan Biyani, Canada

Dr. Vivekanand Jha, Chandigarh

INTERNATIONAL FACULTY

SCIENTIFIC HIGHLIGHTS

NATIONAL FACULTYDr. A.M. Bhagwati

Dr. Dilip Kirpalani

Dr. G.S. Wander

Dr. Hardik Shah

Dr. Mangesh Tiwaskar

Dr. Manisha Sahay

Dr. Mohan Rajapurkar

Dr. N.F. Shah

Dr. Nihar Mehta

Dr. Nimish Shah

Dr. Sana Sahigara

Dr. Santosh Salagre

Dr. Yash Shah


Workshop on Measurement of Blood Pressure

Role of Sacubritil / Valsartan in Hypertension and Heart Failure

Aldosterone Antagonism / Pathway 2

Epidemiology Oration : Current Status of Hypertension and CKD in India

New Antihypertensives

Renal Denervation, Baroreflex Stimulation and Automonic Nervous System in Hypertension

Newer Devices and Strategies for BP Control

Hypertension in Pediatric Population

Keynote Address : Cost Effective Strategies for BP Control in India

Resistant Hypertension

Renovascular Hypertension and Role of CO2 Angiography of Renal Arteries

Concept of HI (Health Incubator) Lab and Speciality Hypertension Clinics

U N Mehta Oration

P J Mehta Young Investigator Award

Dr. Atul Pathak, France

Dr. Gregory Hundemer, Canada

Dr. George Thomas, USA

Dr. Hemant Kulkarni, Australia

Dr. Mohan Biyani, Canada

Dr. Vivekanand Jha, Chandigarh

INTERNATIONAL FACULTY

SCIENTIFIC HIGHLIGHTS

NATIONAL FACULTYDr. A.M. Bhagwati

Dr. Dilip Kirpalani

Dr. G.S. Wander

Dr. Hardik Shah

Dr. Mangesh Tiwaskar

Dr. Manisha Sahay

Dr. Mohan Rajapurkar

Dr. N.F. Shah

Dr. Nihar Mehta

Dr. Nimish Shah

Dr. Sana Sahigara

Dr. Santosh Salagre

Dr. Yash Shah


Documents

Clinical Journal of Hypertension · respectively. A higher proportion of patients with uncontrolled T2DM and HTN reported depression than those with controlled T2DM and HTN (T2DM: