Pub Date : 2020-02-11DOI: 10.2174/1876526202012010001
M. Bijani, Banafsheh Tehranineshat, Fatemeh Ahrari, N. Beygi
Department of Medical-Surgical Nursing, School of Nursing, Fasa University of Medical Sciences, Fasa, Iran Department of Nursing and Community Based Psychiatric Care Research Center , School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran Department of Medical Surgical Nursing, Fasa University of Medical Sciences, Fasa, Iran
{"title":"A Comparison between Multimedia and Traditional Education in Encouraging Adherence to Treatment Regimen in Patients with Hypertension","authors":"M. Bijani, Banafsheh Tehranineshat, Fatemeh Ahrari, N. Beygi","doi":"10.2174/1876526202012010001","DOIUrl":"https://doi.org/10.2174/1876526202012010001","url":null,"abstract":"Department of Medical-Surgical Nursing, School of Nursing, Fasa University of Medical Sciences, Fasa, Iran Department of Nursing and Community Based Psychiatric Care Research Center , School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran Student Research Committee, Fasa University of Medical Sciences, Fasa, Iran Department of Medical Surgical Nursing, Fasa University of Medical Sciences, Fasa, Iran","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47098867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The importance of the arterial blood pressure pulse has been recognized since ancient times, and from then to the present, the interaction of the observer and the patient has progressed in gradual steps. It evolved from the presence of a palpable arterial pulse, being accepted as a sign of life and health condition, to the registration of the features of the arterial pulse as the first ever graphical representation of any physiological parameter in medicine, culminating in the quantification of the tension in the arterial wall as a measurement of arterial “blood pressure.”[1] The current acceptance of high blood pressure (hypertension) as a major cardiovascular risk can claim to have part of its origins in the actuarial and data gathering endeavors of life insurance companies.[2] The ubiquitous use of the brachial cuff sphygmomanometer in the early 20th century enabled collection of numerical data on blood pressure over long periods. The accumulation of blood pressure measurements also enabled data to be collected across the whole human life span. This demonstrated that in the otherwise healthy population, that is, in the normal population with no symptoms of overt ill health, there was a wide range of blood pressure values. Systolic blood pressure varied much more than diastolic blood pressure but increased with age. Since blood pressure was thought to be related to (and drive) tissue and organ perfusion, the marked increase in blood pressure was thought to be essential for adequate blood flow, as is required for efficient organ function. Hence, the concept of “essential hypertension”[3] was used to describe this condition of elevated blood pressure as being due to the essential readjustment of the cardiovascular system to accommodate age-related changes that occur in the vasculature (such as reduced capillary density with sequelae of increased peripheral resistance, hence requiring a higher pressure for adequate tissue perfusion). However, calculations of risk of morbidity and mortality (perhaps related to the forecasting of life insurance premiums) showed that those with elevated diastolic pressure were at higher risk of clinical and multiorgan complications affecting their health. Hence, the accepted notion of how to qualitatively understand elevated blood pressure was that it was essential that mean blood pressure would increase with age (leading to essential hypertension, with no overt symptoms or identifiable cause), that systolic pressure was mainly related to the strength of cardiac contraction (and so related to stroke volume), and that hypertension-related health complications were mainly associated with high diastolic pressure,[4] presumably as diastolic pressure was thought to be more closely associated with total peripheral vascular resistance. However, with accumulation of information from many large epidemiological studies in the latter part of the 20th century, and in particular with longitudinal and generational data from the Fr
{"title":"Hypertension Journal - MQ Special Issue","authors":"E. Barin, A. Avolio","doi":"10.15713/INS.JOHTN.0193","DOIUrl":"https://doi.org/10.15713/INS.JOHTN.0193","url":null,"abstract":"The importance of the arterial blood pressure pulse has been recognized since ancient times, and from then to the present, the interaction of the observer and the patient has progressed in gradual steps. It evolved from the presence of a palpable arterial pulse, being accepted as a sign of life and health condition, to the registration of the features of the arterial pulse as the first ever graphical representation of any physiological parameter in medicine, culminating in the quantification of the tension in the arterial wall as a measurement of arterial “blood pressure.”[1] The current acceptance of high blood pressure (hypertension) as a major cardiovascular risk can claim to have part of its origins in the actuarial and data gathering endeavors of life insurance companies.[2] The ubiquitous use of the brachial cuff sphygmomanometer in the early 20th century enabled collection of numerical data on blood pressure over long periods. The accumulation of blood pressure measurements also enabled data to be collected across the whole human life span. This demonstrated that in the otherwise healthy population, that is, in the normal population with no symptoms of overt ill health, there was a wide range of blood pressure values. Systolic blood pressure varied much more than diastolic blood pressure but increased with age. Since blood pressure was thought to be related to (and drive) tissue and organ perfusion, the marked increase in blood pressure was thought to be essential for adequate blood flow, as is required for efficient organ function. Hence, the concept of “essential hypertension”[3] was used to describe this condition of elevated blood pressure as being due to the essential readjustment of the cardiovascular system to accommodate age-related changes that occur in the vasculature (such as reduced capillary density with sequelae of increased peripheral resistance, hence requiring a higher pressure for adequate tissue perfusion). However, calculations of risk of morbidity and mortality (perhaps related to the forecasting of life insurance premiums) showed that those with elevated diastolic pressure were at higher risk of clinical and multiorgan complications affecting their health. Hence, the accepted notion of how to qualitatively understand elevated blood pressure was that it was essential that mean blood pressure would increase with age (leading to essential hypertension, with no overt symptoms or identifiable cause), that systolic pressure was mainly related to the strength of cardiac contraction (and so related to stroke volume), and that hypertension-related health complications were mainly associated with high diastolic pressure,[4] presumably as diastolic pressure was thought to be more closely associated with total peripheral vascular resistance. However, with accumulation of information from many large epidemiological studies in the latter part of the 20th century, and in particular with longitudinal and generational data from the Fr","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75729900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
There is also a lot of emphasis in the last decade about BP measurement techniques. BP measurement by automated BP instruments or Abstract Chronic kidney disease (CKD) is highly prevalent globally and is strongly associated with cardiovascular disease (CVD). Hypertension affects the vast majority of patients with CKD and increases the risk of CVD, end-stage kidney disease, and mortality. Control of hypertension in CKD is very important in our clinical practice to slow the progression of CKD as well as to reduce CVD risk. Over the past 10 years, three major guidelines have dealt with blood pressure (BP) thresholds and targets for antihypertensive drug therapy in CKD patients: The 2012 Kidney Disease: Improving Global Outcomes Clinical Practice Guideline for the management of BP in CKD; the 2017 American College of Cardiology/American Heart Association 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults; and the 2018 European Society of Cardiology and the European Society of Hypertension guidelines for the Management of arterial hypertension. These guidelines do not offer a consensus on optimal BP targets and have varying recommendations for BP goals in patients with CKD. It may leave practicing physicians and patients in a dilemma. Therefore, it is necessary to understand the existing evidence used to create these guidelines to deliver personalized management and achieve BP targets in CKD.
{"title":"Target Blood Pressure Goals in Patients with Chronic Kidney Disease: Where Do We Stand in this Era of Evidence based Medicine?","authors":"S. Nagaraju, S. Shenoy","doi":"10.15713/ins.johtn.0212","DOIUrl":"https://doi.org/10.15713/ins.johtn.0212","url":null,"abstract":"There is also a lot of emphasis in the last decade about BP measurement techniques. BP measurement by automated BP instruments or Abstract Chronic kidney disease (CKD) is highly prevalent globally and is strongly associated with cardiovascular disease (CVD). Hypertension affects the vast majority of patients with CKD and increases the risk of CVD, end-stage kidney disease, and mortality. Control of hypertension in CKD is very important in our clinical practice to slow the progression of CKD as well as to reduce CVD risk. Over the past 10 years, three major guidelines have dealt with blood pressure (BP) thresholds and targets for antihypertensive drug therapy in CKD patients: The 2012 Kidney Disease: Improving Global Outcomes Clinical Practice Guideline for the management of BP in CKD; the 2017 American College of Cardiology/American Heart Association 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High BP in Adults; and the 2018 European Society of Cardiology and the European Society of Hypertension guidelines for the Management of arterial hypertension. These guidelines do not offer a consensus on optimal BP targets and have varying recommendations for BP goals in patients with CKD. It may leave practicing physicians and patients in a dilemma. Therefore, it is necessary to understand the existing evidence used to create these guidelines to deliver personalized management and achieve BP targets in CKD.","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83118421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hypertension is defined as blood pressure above 140/90 mmHg and is a leading cause for the development of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).[1] Although equally prevalent in both the forms of heart failure, it remains more common in HFpEF patients with prevalence of up to 90%, compared to HFrEF.[2-4] Various guidelines have recommended not only different staging systems for hypertension but also the target blood pressure (BP) goals and therapeutic drug usage in specified populations. Although the target BP goals and therapeutic strategies for BP control in HF patients have been mentioned in different guidelines, robust data are still lacking. Most of the recommendations for optimal BP control in HF patients have been extrapolated from other high-risk populations where intensive BP control showed better long-term cardiovascular (CV) outcomes, however, at an increased risk of adverse effects. Chronic hypertension causes pressure overload leading to ventricular hypertrophy which is initial compensatory mechanism and preserves cardiac output. Subsequently, the left ventricle (LV) dilates as remodeling occurs and LV starts to decompensate. Remodeling occurs due to activation of reninangiotensin system, sympathetic nervous system, and deposition of extracellular matrix. Diastolic dysfunction or the so-called HFpEF is the primary manifestation of hypertensive heart failure. It is only in the later stages that dilated cardiomyopathy leading to HFrEF sets in. Long-term prognosis is poor with increased mortality in hypertensive patients with HF. Treating hypertension can significantly reduce incident of HF and HF hospitalization, especially in old population.[5-7]
{"title":"Hypertension and Heart Failure","authors":"M. Rao, S. Dhanse","doi":"10.15713/INS.JOHTN.0210","DOIUrl":"https://doi.org/10.15713/INS.JOHTN.0210","url":null,"abstract":"Hypertension is defined as blood pressure above 140/90 mmHg and is a leading cause for the development of heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF).[1] Although equally prevalent in both the forms of heart failure, it remains more common in HFpEF patients with prevalence of up to 90%, compared to HFrEF.[2-4] Various guidelines have recommended not only different staging systems for hypertension but also the target blood pressure (BP) goals and therapeutic drug usage in specified populations. Although the target BP goals and therapeutic strategies for BP control in HF patients have been mentioned in different guidelines, robust data are still lacking. Most of the recommendations for optimal BP control in HF patients have been extrapolated from other high-risk populations where intensive BP control showed better long-term cardiovascular (CV) outcomes, however, at an increased risk of adverse effects. Chronic hypertension causes pressure overload leading to ventricular hypertrophy which is initial compensatory mechanism and preserves cardiac output. Subsequently, the left ventricle (LV) dilates as remodeling occurs and LV starts to decompensate. Remodeling occurs due to activation of reninangiotensin system, sympathetic nervous system, and deposition of extracellular matrix. Diastolic dysfunction or the so-called HFpEF is the primary manifestation of hypertensive heart failure. It is only in the later stages that dilated cardiomyopathy leading to HFrEF sets in. Long-term prognosis is poor with increased mortality in hypertensive patients with HF. Treating hypertension can significantly reduce incident of HF and HF hospitalization, especially in old population.[5-7]","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74661226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hypertension is both a leading etiology of end-stage renal disease (ESRD) and a well-recognized cardiovascular risk factor in ESRD patients on dialysis. Despite this, hypertension remains highly prevalent and is often inadequately controlled in this population.[1,2] The prevalence estimates of hypertension in ESRD are quite variable, due to the lack of a standard definition for diagnosis as well as the setting and technique of blood pressure (BP) measurement. Hypertension and chronic kidney disease (CKD) are indeed closely interrelated clinical conditions such that sustained uncontrolled hypertension can cause worsening of renal function and vice versa. Here, we will consider the diagnosis and treatment of hypertension in ESRD patients on renal replacement therapy including both nonpharmacologic and pharmacologic approaches.
{"title":"Hypertension in End-Stage Renal Disease","authors":"Sonali Gupta, S. Liebman","doi":"10.15713/ins.johtn.0177","DOIUrl":"https://doi.org/10.15713/ins.johtn.0177","url":null,"abstract":"Hypertension is both a leading etiology of end-stage renal disease (ESRD) and a well-recognized cardiovascular risk factor in ESRD patients on dialysis. Despite this, hypertension remains highly prevalent and is often inadequately controlled in this population.[1,2] The prevalence estimates of hypertension in ESRD are quite variable, due to the lack of a standard definition for diagnosis as well as the setting and technique of blood pressure (BP) measurement. Hypertension and chronic kidney disease (CKD) are indeed closely interrelated clinical conditions such that sustained uncontrolled hypertension can cause worsening of renal function and vice versa. Here, we will consider the diagnosis and treatment of hypertension in ESRD patients on renal replacement therapy including both nonpharmacologic and pharmacologic approaches.","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89431360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The retina provides a unique opportunity to assess the systemic circulation in vivo and has long been recognized as an important site for identifying systemic vascular changes in disorders such as hypertension and diabetes. The progressive changes in the vessels occurring in hypertension are readily visible and the accompanying hemorrhages, exudates and infarcts have been described as early as 1939 in a grading system for hypertensive retinopathy by Keith-Wagener-Baker (the KWB system).[1] More recently this has been simplified to a 3-step grading system by Mitchell and Wong,[2] which has been suggested to be easier to apply in practice [Table 1].[3,4] The pathophysiology of sustained hypertension involves initially a vasoconstriction of the retinal arteries, followed by progressive thickening of the elastic lamina and hyaline degeneration.[5] This may be recognized on fundoscopy as focal narrowing of vessels, arteriovenous crossing changes (referred to as “nipping or nicking”) where the hardened artery compresses the vein as it crosses with a shared adventitia, and a progressive change in the vessel wall reflectivity termed copper wiring and silver wiring. With sustained hypertension, small hemorrhages, focal areas of infarction (“cotton-wool spots” – so-called because of their white appearance), as well as lipid exudates from break-down of the blood retinal barrier occur. Lipids can form a visible “macular star” pattern. These changes occur in the inner retinal circulation which is derived from the central retinal artery. The choroid, which is the deeper vascular layer of the eye directly beneath the retina supplying the photoreceptors, derives its circulation from the long and short posterior ciliary arteries, which branch from the ophthalmic artery. In severe hypertension, choroidal changes can also occur,[6,7] including choroidal infarcts (represented as Elschnig’s spots – seen as pale, yellow lesions) and pigmentation lines along the larger choroidal vessels (termed Siegrist streaks). Severe hypertension can also lead to optic disc swelling through raised intracranial pressure and optic disc ischemia – termed hypertensive optic neuropathy, and this stage has been termed “malignant hypertension.” The risk of stroke and systemic organ damage is high at this stage, as discussed below. Abstract
{"title":"Hypertension and the Eye","authors":"S. Graham, Angela M Schulz","doi":"10.15713/INS.JOHTN.0198","DOIUrl":"https://doi.org/10.15713/INS.JOHTN.0198","url":null,"abstract":"The retina provides a unique opportunity to assess the systemic circulation in vivo and has long been recognized as an important site for identifying systemic vascular changes in disorders such as hypertension and diabetes. The progressive changes in the vessels occurring in hypertension are readily visible and the accompanying hemorrhages, exudates and infarcts have been described as early as 1939 in a grading system for hypertensive retinopathy by Keith-Wagener-Baker (the KWB system).[1] More recently this has been simplified to a 3-step grading system by Mitchell and Wong,[2] which has been suggested to be easier to apply in practice [Table 1].[3,4] The pathophysiology of sustained hypertension involves initially a vasoconstriction of the retinal arteries, followed by progressive thickening of the elastic lamina and hyaline degeneration.[5] This may be recognized on fundoscopy as focal narrowing of vessels, arteriovenous crossing changes (referred to as “nipping or nicking”) where the hardened artery compresses the vein as it crosses with a shared adventitia, and a progressive change in the vessel wall reflectivity termed copper wiring and silver wiring. With sustained hypertension, small hemorrhages, focal areas of infarction (“cotton-wool spots” – so-called because of their white appearance), as well as lipid exudates from break-down of the blood retinal barrier occur. Lipids can form a visible “macular star” pattern. These changes occur in the inner retinal circulation which is derived from the central retinal artery. The choroid, which is the deeper vascular layer of the eye directly beneath the retina supplying the photoreceptors, derives its circulation from the long and short posterior ciliary arteries, which branch from the ophthalmic artery. In severe hypertension, choroidal changes can also occur,[6,7] including choroidal infarcts (represented as Elschnig’s spots – seen as pale, yellow lesions) and pigmentation lines along the larger choroidal vessels (termed Siegrist streaks). Severe hypertension can also lead to optic disc swelling through raised intracranial pressure and optic disc ischemia – termed hypertensive optic neuropathy, and this stage has been termed “malignant hypertension.” The risk of stroke and systemic organ damage is high at this stage, as discussed below. Abstract","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80480381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The benefits of blood pressure (BP) lowering treatment for the prevention of cardiovascular disease are well established. However, aggressive control of BP is controversial, as it leads to a reduction in organ perfusion and function, thereby increasing overall morbidity and mortality. An elusive balance is now being sought between deleterious effects of hypotension and protective autoregulatory mechanism. Here, we perform a systematic review of data and the current status of aggressive control of BP in various clinical settings.
{"title":"Newer and Aggressive Blood Pressure Goals to Treat Hypertension","authors":"P. Sanzgiri, K. Reddy","doi":"10.15713/ins.johtn.0188","DOIUrl":"https://doi.org/10.15713/ins.johtn.0188","url":null,"abstract":"The benefits of blood pressure (BP) lowering treatment for the prevention of cardiovascular disease are well established. However, aggressive control of BP is controversial, as it leads to a reduction in organ perfusion and function, thereby increasing overall morbidity and mortality. An elusive balance is now being sought between deleterious effects of hypotension and protective autoregulatory mechanism. Here, we perform a systematic review of data and the current status of aggressive control of BP in various clinical settings.","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79978299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The prevalence of hypertension (HTN) in women is an increasing concern. Data from 5,26,336 participants aged 40–79 years in the high-income countries have shown a prevalence of HTN across all women participants aged 40–79 years from 33% to 52%. In the age group of 40–49 years, HTN prevalence ranged from 12% to 20% and in 70–79 years from 61% to 82%.[1] Blood pressure (BP) was recorded for 180,335 participants with a mean age 40.6 ± 14.9 years in India which included 33.2% of women. The prevalence among women was 23.7%. Higher predisposition was noted during the menopausal age. In the age group of 45–54 years, the prevalence of HTN was 34.6% with systolic blood pressure (SBP) of 126.7 ± 18.0 mmHg and diastolic blood pressure (DBP) of 80.3 ± 10.9 mmHg.[2,3] HTN in Women
{"title":"Hypertension in Women","authors":"U. Jadhav, V. S. Khilari","doi":"10.15713/ins.johtn.0186","DOIUrl":"https://doi.org/10.15713/ins.johtn.0186","url":null,"abstract":"The prevalence of hypertension (HTN) in women is an increasing concern. Data from 5,26,336 participants aged 40–79 years in the high-income countries have shown a prevalence of HTN across all women participants aged 40–79 years from 33% to 52%. In the age group of 40–49 years, HTN prevalence ranged from 12% to 20% and in 70–79 years from 61% to 82%.[1] Blood pressure (BP) was recorded for 180,335 participants with a mean age 40.6 ± 14.9 years in India which included 33.2% of women. The prevalence among women was 23.7%. Higher predisposition was noted during the menopausal age. In the age group of 45–54 years, the prevalence of HTN was 34.6% with systolic blood pressure (SBP) of 126.7 ± 18.0 mmHg and diastolic blood pressure (DBP) of 80.3 ± 10.9 mmHg.[2,3] HTN in Women","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89947471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Accurate measurement of blood pressure is crucial for identifying and treating hypertension. Hypertension identified in a clinical setting is strongly associated with cardiovascular disease morbidity and mortality.[1] However, blood pressure fluctuates during the day, and office blood pressure readings do not correlate well with 24 h blood pressure values.[2] Therefore, out of office blood pressure measurement has been used to better characterize the true burden of hypertension and predict cardiovascular risk in individual patients. Ambulatory blood pressure monitoring (ABPM) captures out of office blood pressure values and more accurately reflects the total blood pressure load and variability in an individual patient. Here, we will review the predictive value and role of ABPM in clinical practice.
{"title":"Ambulatory Blood Pressure Monitoring","authors":"Janany Sabescumar, Erika R. Drury","doi":"10.15713/ins.johtn.0174","DOIUrl":"https://doi.org/10.15713/ins.johtn.0174","url":null,"abstract":"Accurate measurement of blood pressure is crucial for identifying and treating hypertension. Hypertension identified in a clinical setting is strongly associated with cardiovascular disease morbidity and mortality.[1] However, blood pressure fluctuates during the day, and office blood pressure readings do not correlate well with 24 h blood pressure values.[2] Therefore, out of office blood pressure measurement has been used to better characterize the true burden of hypertension and predict cardiovascular risk in individual patients. Ambulatory blood pressure monitoring (ABPM) captures out of office blood pressure values and more accurately reflects the total blood pressure load and variability in an individual patient. Here, we will review the predictive value and role of ABPM in clinical practice.","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79755372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Globally, cardiovascular disease (CVD) contributes majorly to increased morbidity and mortality. In addition to the research directed toward the development of newer and more effective treatments, there is also serious thought and research toward modifying risk factors for primary and secondary prevention of CVD. In the ongoing search for such modifiable risk factors, obstructive sleep apnea (OSA) is one main risk factors for several CVDs such as hypertension (HTN), cardiac failure (CF), cardiac arrhythmias, and coronary artery disease.[1] In a society, where there is an ever-increasing aging population compounded with the obesity epidemic, OSA prevalence has increased by 30% and thereby its increased association with CVD. OSA is the repeated stoppage of inspiratory airflow due to oropharyngeal obstruction during sleep. It affects 34% of males and 17% of females in the USA.[2] This upper airway obstruction results in lack of oxygen, disturbance to sleep, and adrenergic nervous system stimulation. Consequently, there is a rise in blood pressure with tachycardia, vascular dysfunction, widespread inflammation, and resistance to insulin. All these changes are said to contribute to the development of CVD.[3] A large volume of evidence has accumulated in favor of OSA linking it to drugresistant HTN, coronary artery disease, congestive CF, and atrial fibrillation [Table 1].
{"title":"Obstructive Sleep Apnea, Hypertension, and Cardiovascular Disease","authors":"P. Tampi","doi":"10.15713/ins.johtn.0190","DOIUrl":"https://doi.org/10.15713/ins.johtn.0190","url":null,"abstract":"Globally, cardiovascular disease (CVD) contributes majorly to increased morbidity and mortality. In addition to the research directed toward the development of newer and more effective treatments, there is also serious thought and research toward modifying risk factors for primary and secondary prevention of CVD. In the ongoing search for such modifiable risk factors, obstructive sleep apnea (OSA) is one main risk factors for several CVDs such as hypertension (HTN), cardiac failure (CF), cardiac arrhythmias, and coronary artery disease.[1] In a society, where there is an ever-increasing aging population compounded with the obesity epidemic, OSA prevalence has increased by 30% and thereby its increased association with CVD. OSA is the repeated stoppage of inspiratory airflow due to oropharyngeal obstruction during sleep. It affects 34% of males and 17% of females in the USA.[2] This upper airway obstruction results in lack of oxygen, disturbance to sleep, and adrenergic nervous system stimulation. Consequently, there is a rise in blood pressure with tachycardia, vascular dysfunction, widespread inflammation, and resistance to insulin. All these changes are said to contribute to the development of CVD.[3] A large volume of evidence has accumulated in favor of OSA linking it to drugresistant HTN, coronary artery disease, congestive CF, and atrial fibrillation [Table 1].","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73969705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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