Hypertension Journal

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Volume 3, Number 4, 2017
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EDITORIAL

Madan Lal Brahma Bhatt

PROLOGUE

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:1] [Pages No:0 - 0]

   DOI: 10.5005/jp-htnj-3-4-iv  |  Open Access |  How to cite  | 

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NON TRADITIONAL RISK FACTORS FOR HYPERTENSION

Narsingh Verma, Ajai Singh, Sabir Ali, Manish Yadav

Analysis of Hypertension as a Risk Factor for Osteoarthritis Knee

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:4] [Pages No:167 - 170]

Keywords: Hypertension, Metabolic syndrome, Obesity, Osteoarthritis, Osteoarthritis knee

   DOI: 10.5005/jp-journals-10043-0089  |  Open Access |  How to cite  | 

Abstract

The basic objective of the recent analysis was to study hypertension as a risk factor for osteoarthritis (OA) knee. In this study, totally 155 patients of OA knee, of age more than 40 years, were enrolled for the study. The study was carried out in the Department of Orthopedic Surgery, King George's Medical University (KGMU), Lucknow, Uttar Pradesh, India. According to the diagnostic criteria of the American College of Rheumatology, the cases were taken into consideration. A brief history about the disease was taken, and complete examinations were done. For the clinical severity, visual analog scale (VAS) and Lequesne index were done and for radiological severity assessment, Kellgren–Lawrence (KL) grading and X-ray bilateral knee were done to observe the radiological changes. Moreover, the blood pressure was measured consecutively in both arms for three times via auscultatory method following the American Heart Association guidelines, and the average was calculated and recorded. If the recorded average is greater than 140/90 mm Hg, then the subject is labeled as “hypertensive.” In this study, we found a significant association between the severity of the OA knee and hypertension. The study is not only for our knowledge enrichment about the association of OA and hypertension, but also to fill the gaps with related information; it will reshape our knowledge toward the management of heart disease, hypertension, and OA. Also, we can determine the new possible risk factors for these diseases. How to cite this article Singh A, Verma N, Yadav M, Ali S. Analysis of Hypertension as a Risk Factor for Osteoarthritis Knee. Hypertens J 2017;3(4):167-170.

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PHYSIOLOGY OF BLOOD PRESSURE REGULATION

Narsingh Verma, Arvind K Pal

Effect of Altitude on Blood Pressure

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:2] [Pages No:171 - 172]

Keywords: Altitude, Hypertension, Hypoxia

   DOI: 10.5005/jp-journals-10043-0090  |  Open Access |  How to cite  | 

Abstract

The effect of higher altitude over the blood pressure (BP) is not exactly known, and it appears to vary both between and within individuals. The effects of lower temperature, light, increased physical stress, and duration of living at higher altitude also play a significant role. Most of the studies showed that higher altitude correlated with rising BP. This change in BP is due to many factors, the important one being the effect of hypoxia causing activation of sympathetic nervous system. Activation of sympathetic nervous system causes an increase in cardiac output, heart rate, and peripheral vasoconstriction, which lead to increase in BP. The incidence of BP in high latitudes is controversial; some research shows greater rates while others show lesser rates of hypertension in these individuals. It may be due to the effects of multiple other confounding factors like genetic, ecological, and lifestyle variables. Hence, increasing popularity of high-altitude travel needs further research to evaluate this problem. Furthermore, the implications of altitude-induced hypertension for cardiovascular risk and end-organ damage require more clarification. How to cite this article Verma N, Pal AK. Effect of Altitude on Blood Pressure. Hypertens J 2017;3(4):171-172.

4,757

PHYSIOLOGY OF BLOOD PRESSURE REGULATION

Nibedita Priyadarsini, Sajal C Singh, Sushil C Mahapatra

Central Blood Pressure: Current Evidence and Clinical Importance in Hypertensive Disorders during Pregnancy

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:5] [Pages No:173 - 177]

Keywords: Central blood pressure, Eclampsia, Hypertension, Preeclampsia, Pregnancy-induced hypertension

   DOI: 10.5005/jp-journals-10043-0091  |  Open Access |  How to cite  | 

Abstract

Hypertensive disorders complicate 5 to 10% of all pregnancies and hypertension is a major pregnancy complication associated with both fetal and maternal morbidity and mortality. Measurement of brachial blood pressure (BP) is a routine clinical assessment tool for management of various hypertensive disorders. Systolic pressure varies throughout the vasculature; aortic systolic pressure [or central blood pressure (CBP)] is actually lower than that of systolic BP in brachial artery. Central to peripheral pressure difference is highly variable among individuals. In various studies, it has been reported that CBP is a better predictor of cardiovascular events as compared with peripheral BP. Hypertensive disorders in pregnancy are associated with increased arterial stiffness indices, both during and after pregnancy leading to differences in central and peripheral pressures. In this article, the issues related to importance of CBP measurement for management of hypertensive disorders in pregnancy have been discussed. How to cite this article Priyadarsini N, Singh SC, Goyal M, Mahapatra SC. Central Blood Pressure: Current Evidence and Clinical Importance in Hypertensive Disorders during Pregnancy. Hypertens J 2017;3(4):173-177.

1,362

PHYSIOLOGY OF BLOOD PRESSURE REGULATION

Anuj Maheshwari, Harish Basera

Salt Sensitivity and Hypertension

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:5] [Pages No:178 - 182]

Keywords: Dietary salt, Hypertension, Salt sensitivity

   DOI: 10.5005/jp-journals-10043-0092  |  Open Access |  How to cite  | 

Abstract

Enough evidence is there to link excess salt intake with cardiovascular and renal risks through hypertension though substantial evidence is also there to support that blood pressure is not always responding to salt. A lot of metabolic and neurohormonal factors determine this salt sensitivity in addition to genetic factors that determine substantial excretion of salt, so it may not increase blood pressure despite high intake. Salt-sensitive hypertensives have reduced levels of urinary endothelin, contributing to impaired natriuresis in response to a salt load. Salt load also increases free radicals and paradoxically decreases excretion of nitric oxide metabolites in salt-sensitive individuals. Type 2 diabetic patients with microalbuminuria are more salt sensitive as they have lower urinary excretion of nitric oxide. Nitric oxide deficiency facilitates endothelial dysfunction causing hypertension in salt-sensitive people, impeding vasodilation after salt load. Sympathetic nervous system plays a significant role in maintenance of blood pressure in response to salt through urinary and plasma levels of catecholamine and renal nerve activity. Apart from this, atrial natriuretic peptides (ANPs) and cytochrome P450-derived metabolites of arachidonic acid play significant roles. Insomnia and menopause increase salt sensitivity. Kidney provides sensitive and specific biomarkers for salt sensitivity in the form of proteomics, and renal proximal tubule cells, microribonucleic acid (miRNA), and exosomes are excreted into the urine apart from genetic biomarkers. A J-shaped curve relationship exists between salt intake and mortality. Salt intakes above and below the range of 2.5 to 6.0 gm/day are associated with high cardiovascular risk. Salt restriction can be a cause of hypertension in inverse salt-sensitive people. Available prevalence studies do not differentiate between salt-sensitive and salt-resistant populations, nor do they include normotensive salt-sensitive people who get their blood pressure raised in response to dietary salt. In these circumstances, salt sensitivity arises as an independent risk factor for cardiovascular mortality and morbidity. How to cite this article Maheshwari A, Basera H. Salt Sensitivity and Hypertension. Hypertens J 2017;3(4):178-182.

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HYPERTENSIVE CRISIS

Imran Rizvi, Ravindra K Garg, Hardeep S Malhotra, Manan M Mehta, Ravi Uniyal

Management of Blood Pressure during Acute Stroke: A Narrative Review

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:6] [Pages No:183 - 188]

Keywords: Hypertension, Intracerebral hemorrhage, Ischemic stroke, Labetalol, Nicardipine

   DOI: 10.5005/jp-journals-10043-0093  |  Open Access |  How to cite  | 

Abstract

Hypertension is among the most important risk factors for the occurrence of stroke. Acute stroke patients commonly have an elevated blood pressure (BP), and maintaining an appropriate level of BP is a crucial step in the successful management of acute stroke. In this article, we review various trial and published guidelines for the management of hypertension during intracerebral hemorrhage (ICH) and acute ischemic stroke. Patients with ICH were found to have systolic BP (SBP) in the range of 150 to 220 mm Hg and need acute lowering of SBP to less than 140 mm Hg. It is safe to do so if there are no contraindications. If a patient with ICH presents with an SBP of more than 220 mm Hg, then the BP should be lowered aggressively using intravenous infusion along with frequent monitoring. Patients of acute ischemic stroke, who have BP >185/110 mm Hg, should have their BP rapidly controlled, if they are being considered for thrombolytic therapy. Injectable labetalol, nicardipine, hydralinzine, and enalaprilat are considered appropriate for acute management of elevated BP in patients with acute ischemic stroke. Patients of acute ischemic stroke with SBP > 180 to 230 mm Hg or diastolic BP (DBP) > 105 to 120 mm Hg should receive intravenous labetalol 10 mg; this can be followed by a continuous infusion at the rate of 2 to 8 mg/min, if required. Nicardipine infusion is another alternative that can be uptitrated according to the desired BP levels. For secondary prevention of ischemic stroke, BP lowering can be done after first several days. The SBP > 140 mm Hg and DBP >90 mm Hg should be treated. How to cite this article Rizvi I, Garg RK, Malhotra HS, Kumar N, Mehta MM, Uniyal R, Pandey S. Management of Blood Pressure during Acute Stroke: A Narrative Review. Hypertens J 2017;3(4):183-188.

1,309

NON PHARMACOLOGICAL TREATMENT OF HYPERTENSION

Arvind K Pal

Yoga and Hypertension

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:4] [Pages No:189 - 192]

Keywords: High blood pressure, Lifestyle modification, Yoga

   DOI: 10.5005/jp-journals-10043-0094  |  Open Access |  How to cite  | 

Abstract

High blood pressure (BP) is a major public health problem worldwide. It is an important risk factor for acute myocardial infarction, cerebrovascular disease, chronic renal failure, and congestive heart failure. Lifestyle modifications play an important role in prehypertensive individuals and also act as an adjunct to antihypertensive therapy. Yoga practices have been shown to be effective in reducing BP in hypertensive population. The probable mechanism by which yoga reduces BP is by reduction in sympathetic activity, facilitating autonomic balance, which reduces chemoreceptor responses, and enhancing baroreflex sensitivity. Yoga is also effective as an adjunct therapy in reducing antihypertensive medication use. There is a need for recognition of yoga by our health system as a complementary therapy for treating hypertension (HPT). How to cite this article Tiwari S, Pal AK. Yoga and Hypertension. Hypertens J 2017;3(4):189-192.

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COMMENTARY ON HYPERTENSION GUIDELINES

Mahim Saran, Sudhanshu K Dwivedi

Impact of American College of Cardiology/American Heart Association Guidelines 2017

[Year:2017] [Month:] [Volume:3] [Number:4] [Pages:3] [Pages No:193 - 195]

Keywords: Guidelines, Hypertension, Noncommunicable disease

   DOI: 10.5005/jp-journals-10043-0095  |  Open Access |  How to cite  | 

Abstract

Reduction in the level of blood pressure (BP) from 140/90 to 130/80 mm Hg for defining hypertension is one of the major practice changing modifications of the 2017 American College of Cardiology/American Heart Association guidelines which are bound to have a huge societal impact. The number of hypertension patients will increase 1.5 times after this definition change. Although the BP levels for defining hypertension have changed, the levels at which pharmacological therapy should be started have remained the same, i.e., ≥140/90 mm Hg (Stage 2 hypertension according to newer guidelines) except in special situations (clinical atherosclerotic cardiovascular disease or estimated 10-year cardiovascular disease risk of ≥10%). All in all, definitely these guidelines are more comprehensive, give a much more clarity to the treating physician, and are aimed at better long-term prevention of target-organ damage. But at the same time, they leave us in the same dilemma which arises after every major guideline change: how to deal with patients who are being treated as per the old guidelines? How to cite this article Saran M, Dwivedi SK. Impact of American College of Cardiology/American Heart Association Guidelines 2017. Hypertens J 2017;3(4):193-195.

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