Literature Review On Obesity and Hypertension

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Crafting a literature review on obesity and hypertension can be an arduous task.

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Women, in whom sarcopenia is much more prevalent, exhibit levels of excess of LV mass
substantially greater than men, strongly suggesting, therefore, that there might be alterations in the
normal myocardial structure associated with the increased LV mass. Since the 1933 initial clinical
description of OCM, more than 57,000 articles whose titles include the term obesity and CVD have
been published in PubMed, with the bulk of the studies published towards the end of the 1990s.
Blood pressure treatment - “conventional“ wisdom in ESRD patients. Data abstracted included: (a)
first author name; (b) publication year; (c) patient sample size: (d) mean age of recruited patients; (e)
percentage of female patients; (f) BMI; (g) LVEF; (h) LV mass index; and mean follow-up period.
However, with the prevalence of obesity rapidly rising, research interest on its deleterious effect on
cardiac morphology and function has been on the increase. It is difficult to isolate the effect of
obesity on cardiac function from that of other concomitant and synergistic comorbidities. Relation of
various degrees of body mass index in patients with systemic hypertension to left ventricular mass,
cardiac output, and peripheral resistance (The Hypertension Genetic Epidemiology Network Study).
This puts more strain on the arteries and when this strain is resisted it causes the blood pressure to
rise. For Later 0 ratings 0% found this document useful (0 votes) 67 views 13 pages The
Pathophysiology of Hypertension in Patients With Obesity Uploaded by Luis Daniel Bernal Conde
The Pathophysiology of Hypertension in Patients With Obesity Full description Save Save The
Pathophysiology of Hypertension in Patients Wi. Diabetes obesity in patients with COPD Angelo
Avogaro. Journal of the American College of Cardiology 43: 1399-1404. Bariatric surgery brings
about a significant and long-term change in the weight and also brings about a significant drop in the
blood pressure levels. The purpose of the present review and meta-analysis is to synthesize current
scholarly and practitioner understanding of IOC with a focus on broadening the knowledge on
diagnosis and clinical management. Reviews in Endocrine and Metabolic Disorders 14: 59-68.
Abnormal LV geometry and function can substantially improve after weight loss in both adults and
adolescents. At the heart level, this has been directly demonstrated using cine-magnetic resonance
imaging and a technique called ?localized proton spectroscopy?, able to identify exactly the
triglyceride peak. Selected articles were then abstracted and entered into a data abstraction form to
extract all the salient information for analysis. LV hypertrophy maybe eccentric in normotensive
morbid obese patients or concentric in morbid obese patients with chronic systemic hypertension.
The presence of myocardial fat infiltration does not always cause LV systolic dysfunction because it
is not always present in obesity. In the case of more than one follow-up period, the longest period
was considered (Table 4). HF is classified into Stages A to D, with specific treatment protocols for
each stage. People who have chronic sleep apnoea experience sudden drop in their oxygen levels
thereby increasing the blood flow and putting a pressure on the blood vessels which increases the
blood pressure. With such extraneous factors, research on IOC has been fragmented and at most
inconsistent. Thus, obesity and hypertension together are one of the top reasons forcardiovascular
diseases. Severe obstructive sleep apnea elicits concentric left ventricular geometry. Left ventricular
mass and body size in normotensive children and adults: assessment of allometric relations and
impact of overweight. Thus, the increased LV mass in obesity is related not only to the increased
muscle component, which is elicited by the increased hemodynamic load. The therapeutic target is to
cause weight loss and reverse obesity-associated hemodynamic and structural abnormalities. This
meta-analysis combines findings from current studies on diagnosis of ventricular dysfunction in
OCM patients compared to normal (control) patients. No Disclosures. Idiopathic Intracranial
Hypertension Pseudotumor cerebri.
Fat mass is as important as, and perhaps more important than, fat-free mass to promote increase in
LV mass in visceral obesity, which is especially evident in women, related to their body composition.
However, the initial clinical descriptions of a pathologic obesity-associated cardiac morphology and
dysfunction appeared in 1933. The American Journal of the Medical Sciences 321: 225-236. High
prevalence of hypertension in obese children in the Caribbean. Journal of the American College of
Cardiology 57: 732-739. Heart Disease and Stroke: A Journal for Primary Care Physicians 2: 317-
321. The most assessed echocardiographic parameters related to ventricular structure: LV end-
diastolic volume (LVEDV), LV end-systolic volume (LVESV), relative wall thickness (RWT) and
LV mass. Clinical and Experimental Pharmacology and Physiology 38: 879-887. Additional studies
identified from screening bibliographies and review articles on bariatric surgery. The findings reveal
the safety and efficacy of bariatric surgery as a weight loss intervention for OCM patients or a
bridge to recovery or to heart transplantation. We think that efforts should be oriented to
characterize. Endothelial dysfunction and inflammation of the small vessel wall are important events
in the development of atherosclerosis. Pathophysiologic mechanisms for the development of OCM
include changes in cardiac hemodynamics, myocardial remodeling, ventricular dysfunction;
metabolic disturbances; myocardial lipotoxicity, neurohumoral derangement; and small vessel
disease. Journal of the American College of Cardiology 51: 1775-1783. Relation of obesity and
gender to left ventricular hypertrophy in normotensive and hypertensive adults. The inclusion criteria
for studies included: (a) prospective and retrospective trials; (b) used echocardiography imaging for
diagnosis of ventricular dysfunction; (c) published outcomes on alterations in both ventricular
structure and function; and (d) compared data from obese and controls (lean patients). Despite the
decades-long accumulated evidence of obesity associated heart failure, the recent research interest
on OCM is attributable to the rapidly increasing global prevalence of obesity in the general
population. Normalization for body size and population-attributable risk of left ventricular
hypertrophy: the Strong Heart Study. Studies using CMR imaging demonstrated increased
preciseness compared to echocardiography studies but were fewer because of the ready availability
and ease of use of echocardiography. Thus, obesity and hypertension together are one of the top
reasons forcardiovascular diseases. In fact, your blood pressure rises as your body weight increases.
Fifteen (15) of these studies recruited a prospective cohort while three (3) recruited a retrospective
cohort. It is difficult to isolate the effect of obesity on cardiac function from that of other
concomitant and synergistic comorbidities. Association of left ventricular hypertrophy with
metabolic risk factors: the HyperGEN study. However, although LVESV was higher in obese patients
(42 ml) compared to control (30 ml) the difference was not significant. Aerobic exercise further
contributes to decreasing systolic blood pressure in both hypertensive and normotensive patients.
Effectively controlling BP and reducing hypertensive LVH is difficult without managing obesity.
These extremely alarming global levels and trends of obesity in the general population and its harmful
effect on many different physical and mental conditions together with its involvement in cardiac
diseases explains the renewed research interest in obesity. Surgery for Obesity and Related Diseases
3: 503-507. Abnormal LV geometry and function can substantially improve after weight loss in both
adults and adolescents.
Bariatric surgery causes substantial weight loss to directly decrease obesity and cardiac failure as
well as indirectly decrease metabolic syndrome and comorbidities, and reverse ventricular
remodelling and dysfunction. Factors associated with the prevalence of hypertension in the
southeastern United States: insights from 69,211 blacks and whites in the Southern Community
Cohort Study. Cardiovascular risk in relation to a new classification of hypertensive left ventricular
geometric abnormalities. According to the old paradigm of LV mass only related to fat-free mass,
lower LV mass could be expected in obese individuals with relative fat-free mass deficiency. In
morbid obese patients, cardiomyopathy may result from obesity, which may be potentiated with
increased predisposition to other risk factors such as coronary artery disease, diabetes mellitus,
hypertension, dyslipidemia, insulin resistance, metabolic syndrome, kidney disease, obstructive sleep
apnea and cardiac conduction abnormalities. Journal of the American College of Cardiology 57: 732-
739. Journal of the American College of Cardiology 43: 1399-1404. Obesity and hypertension
together can give rise to an array of health issues and challenges there by affecting health, quality of
life and life expectancy. Diabetes obesity in patients with COPD Angelo Avogaro. The most assessed
echocardiographic parameters related to ventricular structure: LV end-diastolic volume (LVEDV),
LV end-systolic volume (LVESV), relative wall thickness (RWT) and LV mass. Serous Meningitis
(Quincke, 1897) Pseudotumor Cerebri (Nonne, 1904). Blood pressure treatment - “conventional“
wisdom in ESRD patients. LV remodeling contributes to the development of LV hypertrophy and
LV diastolic dysfunction, which may result in biventricular enlargement and systolic dysfunction.
Obesity Research and Clinical Practice 6: e181-e188. The relation of adiposity to blood pressure and
development of hypertension. Obesity and daytime pulse pressure are predictors of left ventricular
hypertrophy in true normotensive individuals. Left ventricular chamber and wall mechanics in the
presence of concentric geometry. An important methodological issue, when assessing blood pressure
in the obese patient, is the cuff size. Obesity Research and Clinical Practice 6: e189-e196. These
changes include statistically significant improvement in LV structure and systolic function. Its
extreme consequence is obesity cardiomyopathy (OCM), a form of non-ischemic dilated
cardiomyopathy occurring in the setting of lipid accumulation in the cardiomyocytes causing
alterations in cardiac structure and function not explained by structural heart diseases or systemic
hypertension. The American Journal of Clinical Nutrition 64: 650-658. Cookie Settings Accept All
Reject All Privacy Policy Manage consent. Considerable debate also persists as to whether isolated
obesity can directly cause cardiomyopathy in humans since its effect on cardiac function and
structure cannot be isolated from those of comorbidities such as hypertension, dyslipidemia, glucose
intolerance and coronary artery disease. Prevalence of all risk factors is significantly reduced in the
managed MetS sub-group (0.05 Full size image. LV hypertrophy maybe eccentric in normotensive
morbid obese patients or concentric in morbid obese patients with chronic systemic hypertension.
Which cuff size is preferable for blood pressure monitoring in most hypertensive patients. A lower
estimated glomerular filtration rate (GFR) was associated with a higher incidence of various
cardiovascular outcomes. High blood pressure in overweight and obese youth: implications for
screening. The American Journal of the Medical Sciences 321: 225-236.
Journal of the American College of Cardiology 54: 718-726. The statistical effect of adipose mass on
variability of LV mass in women is interrelated to the visceral distribution, as indicated by the
significant impact of waist-to-hip ratio (Fig. 3 ). Fig. 3 Relative contribution of parameters
associated with variance of LV mass index, by standardized ?-coefficients obtained by multiple
linear regression analysis in the cohort of the Strong Heart Study. Even in the presence of good
control of BP, not necessarily LV mass follows the decrease in BP when obesity is present. Apart
from just weight and obesity the fat distribution is also an important factor that plays a major role.
Obesity-related hypertension: pathogenesis, cardiovascular risk, and treatment. The guidelines
classified HF in to Stages A to D and recommends specific therapy for each stage, which include
conventional HF therapy for OCM patients should include prophylactic (healthy living - targeting
weight loss), pharmacological support, device therapy, and heart transplantation ( Figure 4 ). We
think that efforts should be oriented to characterize. Note that prevalence of LV hypertrophy follows
the excess of adipose mass, more than BP or LV chamber dimension. OUTLINE OF THE
LECTURE Metabolism and regulations Hyponutrition (kwashiorkor, marasmus) Obesity.
Metabolism. In addition, pure obesity in the absence of hypertension, dyslipidemia, glucose
intolerance and CAD is very rare, and therefore, difficult to isolate the deleterious cardiac effects of
these comorbid disease entities from that caused exclusively by obesity. Left ventricular geometry in
obesity: is it what we expect. Left ventricular mass correlates with fat-free mass but not fat mass in
adults. Aerobic exercise further contributes to decreasing systolic blood pressure in both
hypertensive and normotensive patients. Thus, obesity and hypertension together are one of the top
reasons forcardiovascular diseases. Since the 1933 initial clinical description of OCM, more than
57,000 articles whose titles include the term obesity and CVD have been published in PubMed, with
the bulk of the studies published towards the end of the 1990s. Abnormal conditions associated with
cardiovascular modifications in obesity Hemodynamic load Two conditions are frequent in obesity,
potentially helping explaining the prevalent concentric LV geometry: severe obstructive sleep apnea
(OSA) and masked hypertension. The exclusion criteria included (a) non-human studies; (b) non-
surgical weight loss interventions; (c) case reports; (d) letters and comments; and (e) studies with
follow-up of less than one month. Although OCM has been documented in rodent models, it is
unclear whether isolated obesity can directly lead to cardiomyopathy in humans. This meta-analysis
goes further to combine recent research findings to determine the efficacy of bariatric surgery in
reducing BMI and its effect on cardiac structure and function. The restrictive type refers to surgical
reduction of the size of the stomach leading to food intolerance and subsequently weight loss.
Considerable debate also persists as to whether isolated obesity can directly cause cardiomyopathy in
humans since its effect on cardiac function and structure cannot be isolated from those of
comorbidities such as hypertension, dyslipidemia, glucose intolerance and coronary artery disease.
Cardiovascular modifications of obesity Evaluation of obesity-related cardiovascular changes poses
method problems, especially when normalization for body size is needed. Impact and pitfalls of
scaling of left ventricular and atrial structure in population-based studies. Ideal Obesity Clinic for
out-patient care with the latest state-of-art infrastructure in Operation Theatres. The prevalence was
lower but still very high on other parts of the world. Pre and post BMI, pre and post LV function
(LVEF), and pre and post LV structure (LV mass index). The presence of comorbidities such as
hypertension, diabetes mellitus, dyslipidemia, insulin resistance, metabolic syndrome, obstructive
sleep apnea and kidney diseases may accelerate or potentiate the development of OCM in morbid
obese patients. Obesity exaggerates LV response to increased hemodynamic load in large part
throughout the effect of non-hemodynamic mechanisms elicited by visceral adiposity. The mean LV
mass was higher in obese patients (199 g, range 161 to 240 g) compared to control (144 g, range 128
to 163 g). The relation of adiposity to blood pressure and development of hypertension.
Its extreme consequence is obesity cardiomyopathy (OCM), a form of non-ischemic dilated
cardiomyopathy occurring in the setting of lipid accumulation in the cardiomyocytes causing
alterations in cardiac structure and function not explained by structural heart diseases or systemic
hypertension. The prevalence was lower but still very high on other parts of the world. Apart from
just weight and obesity the fat distribution is also an important factor that plays a major role. He is a
director of Laparo Obeso Centre which is a centre for treatment for weight loss and weight-related
metabolic diseases. This kind of a situation can be a silent killer as they could lead to serious
complications like stroke or heart attack. Surgery for Obesity and Related Diseases 5: 648-652.
Abnormal LV geometry and function can substantially improve after weight loss in both adults and
adolescents. A lower estimated glomerular filtration rate (GFR) was associated with a higher
incidence of various cardiovascular outcomes. Download citation Received: 03 August 2016
Accepted: 22 November 2016 Published: 30 November 2016 DOI: Share this article Anyone you
share the following link with will be able to read this content: Get shareable link Sorry, a shareable
link is not currently available for this article. In Pediatric Metabolic Syndrome (pp. 199-215).
Springer, London. But opting out of some of these cookies may affect your browsing experience.
The guidelines classified HF in to Stages A to D and recommends specific therapy for each stage,
which include conventional HF therapy for OCM patients should include prophylactic (healthy
living - targeting weight loss), pharmacological support, device therapy, and heart transplantation (
Figure 4 ). Serous Meningitis (Quincke, 1897) Pseudotumor Cerebri (Nonne, 1904). Kirchner Canton
Medical Education Foundation, Canton, OH Find this author on Google Scholar Find this author on
PubMed Search for this author on this site For correspondence. Obesity and hypertension together
can give rise to an array of health issues and challenges there by affecting health, quality of life and
life expectancy. The therapeutic target is to cause weight loss and reverse obesity-associated
hemodynamic and structural abnormalities. Alterations of left ventricular myocardial characteristics
associated with obesity. Both eccentric and concentric LV hypertrophy occur in obese individuals.
Out of these, the cookies that are categorized as necessary are stored on your browser as they are
essential for the working of basic functionalities of the website. With such extraneous factors,
research on IOC has been fragmented and at most inconsistent. Obesity Research and Clinical
Practice 6: e189-e196. Although OCM has been documented in rodent models, it is unclear whether
isolated obesity can directly lead to cardiomyopathy in humans. No Disclosures. Idiopathic
Intracranial Hypertension Pseudotumor cerebri. Cardiovascular syndromes X, endothelial
dysfunction and insulin resistance. Thus, obesity and hypertension together are one of the top
reasons forcardiovascular diseases. Criteria for inclusion included studies that: (a) were prospective
or retrospective cohort clinical trials; (b) recruited obese patients symptomatic of heart failure; (c)
followed patients for at least three (3) months; (d) investigated bariatric surgery; and (e) provided
quantifiable outcomes including at least one of the following. The initial mention of excess
deposition of fat involving the heart of obese individuals was in 1783. This diagram schematically
represents hemodynamic changes resulting from excessive adipose accumulation in morbid obese
patients and their subsequent effect on cardiac morphology and ventricular function and eventually
heart failure. Thus, this review article aggregates current research findings and practitioner
knowledge on the clinical status of obesity cardiomyopathy including two meta-analyses of its
diagnosis and clinical management methods. Left ventricular mass correlates with fat-free mass but
not fat mass in adults.
These changes include statistically significant improvement in LV structure and systolic function.
Prepared by the CHEP Implementation Task Force in collaboration with. In Pediatric Metabolic
Syndrome (pp. 199-215). Springer, London. This meta-analysis combines findings from current
studies on diagnosis of ventricular dysfunction in OCM patients compared to normal (control)
patients. Obesity-associated epicardial fat extension into the ventricular and atrial myocardium may
result in fatty infiltration in the RV and perivascular regions. Its extreme consequence is obesity
cardiomyopathy (OCM), a form of non-ischemic dilated cardiomyopathy occurring in the setting of
lipid accumulation in the cardiomyocytes causing alterations in cardiac structure and function not
explained by structural heart diseases or systemic hypertension. Association of suboptimal blood
pressure control with body size and metabolic abnormalities. Report this Document Download now
Save Save The Pathophysiology of Hypertension in Patients Wi. Alterations of left ventricular
myocardial characteristics associated with obesity. For Later 0 ratings 0% found this document
useful (0 votes) 67 views 13 pages The Pathophysiology of Hypertension in Patients With Obesity
Uploaded by Luis Daniel Bernal Conde The Pathophysiology of Hypertension in Patients With
Obesity Full description Save Save The Pathophysiology of Hypertension in Patients Wi. Upload
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Next What is Scribd. Pathophysiologic mechanisms for the development of OCM include changes in
cardiac hemodynamics, myocardial remodeling, ventricular dysfunction; metabolic disturbances;
myocardial lipotoxicity, neurohumoral derangement; and small vessel disease. Serous Meningitis
(Quincke, 1897) Pseudotumor Cerebri (Nonne, 1904). Left ventricular geometry in obesity: is it what
we expect. Dr. Zahoor Ali Shaikh. Hypertension. 1. Essential hypertension (90-95%) 2. Effectively
controlling BP and reducing hypertensive LVH is difficult without managing obesity. We also use
third-party cookies that help us analyze and understand how you use this website. These extremely
alarming global levels and trends of obesity in the general population and its harmful effect on many
different physical and mental conditions together with its involvement in cardiac diseases explains
the renewed research interest in obesity. HF is classified into Stages A to D, with specific treatment
protocols for each stage. Relations of left ventricular mass to fat-free and adipose body mass: the
strong heart study. But opting out of some of these cookies may affect your browsing experience.
Studies were identified using a combination of the following key words: ventricular function,
obesity, obese, body mass index (BMI) and echocardiography. In obese rat models, defects in lipid
oxidation (mismatch between FFA uptake and use) causes the accumulation of FFA and TG in
cardiomyocytes causing ventricular hypertrophy and dysfunction. Bariatric surgery causes substantial
weight loss to directly decrease obesity and cardiac failure as well as indirectly decrease metabolic
syndrome and comorbidities, and reverse ventricular remodelling and dysfunction. Based on these
findings, one might postulate that visceral fat contributes by non-hemodynamic pathways to the
development of concentric LV geometry in obese individuals. Data abstracted included: (a) first
author name; (b) publication year; (c) patient sample size: (d) mean age of recruited patients; (e)
percentage of female patients; (f) BMI; (g) LVEF; (h) LV mass index; and mean follow-up period.
Thus, obesity and hypertension together are one of the top reasons forcardiovascular diseases. The
clinical target is to reduce myocardial adiposity and consequently achieve a reversal in ventricular
remodeling and minimize the risk of developing comorbidities. Two conditions with elevated
hemodynamic impact, severe obstructive sleep apnea and masked hypertension contribute to the
development of such a geometric pattern, but non-hemodynamic factors, and specifically body
composition, also influence prevalence of concentric LV geometry. Depressed myocardial energetic
efficiency is associated with increased cardiovascular risk in hypertensive left ventricular
hypertrophy.
Differences in RWT between obese patients and control were also not significant. Reversibility of
cardiac abnormalities in morbidly obese adolescents. Interleukin-6, C-reactive peptide and TNF are
associated with heart failure and subclinical LV dysfunction. This meta-analysis goes further to
combine recent research findings to determine the efficacy of bariatric surgery in reducing BMI and
its effect on cardiac structure and function. Journal of the American College of Cardiology 53: 1925-
1932. Both eccentric and concentric LV hypertrophy occur in obese individuals. Journal of
Cardiopulmonary Rehabilitation and Prevention 23: 61-169. Thus, the measure of LV mass in obese
individuals includes cell populations and cell components that are different from what measured in
lean subjects. Either conditions influence development of left ventricular (LV) hypertrophy (LVH),
through different biological and hemodynamic mechanisms: obesity is conventionally thought to
elicit a coherent growth of LV chamber dimensions and myocardial wall thickness (eccentric LV
geometry), whereas a more accentuated increase in wall-thickness (concentric LV geometry) is
attributed to hypertension. Pathophysiologic mechanisms for the development of OCM include
changes in cardiac hemodynamics, myocardial remodeling, ventricular dysfunction; metabolic
disturbances; myocardial lipotoxicity, neurohumoral derangement; and small vessel disease. Journal
of the American College of Cardiology 57: 1368-1374. In morbid obese patients, cardiomyopathy
may result from obesity, which may be potentiated with increased predisposition to other risk factors
such as coronary artery disease, diabetes mellitus, hypertension, dyslipidemia, insulin resistance,
metabolic syndrome, kidney disease, obstructive sleep apnea and cardiac conduction abnormalities.
Current treatment protocols target the underlying causes of obesity (weight loss) and heart failure.
The relation of adiposity to blood pressure and development of hypertension. Sex differences in
obesity-related changes in left ventricular morphology: the Strong Heart Study. Hemodialysis
Symposium 08-09 February 2014 Al Madinah AlMunawwarah. Criteria for inclusion included
studies that: (a) were prospective or retrospective cohort clinical trials; (b) recruited obese patients
symptomatic of heart failure; (c) followed patients for at least three (3) months; (d) investigated
bariatric surgery; and (e) provided quantifiable outcomes including at least one of the following.
Current studies and meta-analysis have shown bariatric surgery achieves a greater weight loss in
comparison to non-surgical (dietary or pharmacological) interventions. Target organ damage in “white
coat hypertension” and “masked hypertension”. Cardiovascular syndromes X, endothelial
dysfunction and insulin resistance. Surgery for Obesity and Related Diseases 5: 648-652. Blood
pressure treatment - “conventional“ wisdom in ESRD patients. Use of this website is subject to the
website terms of use and privacy policy. Studies using CMR imaging demonstrated increased
preciseness compared to echocardiography studies but were fewer because of the ready availability
and ease of use of echocardiography. Although OCM has been documented in rodent models, it is
unclear whether isolated obesity can directly lead to cardiomyopathy in humans. Elevated C-reactive
protein in patients with obstructive sleep apnea. Journal of the American College of Cardiology 54:
718-726. Association of left ventricular hypertrophy with metabolic risk factors: the HyperGEN
study. Impact of obesity on cardiac geometry and function in a population of adolescents: the Strong
Heart Study. Its extreme consequence is obesity cardiomyopathy (OCM), a form of non-ischemic
dilated cardiomyopathy occurring in the setting of lipid accumulation in the cardiomyocytes causing
alterations in cardiac structure and function not explained by structural heart diseases or systemic
hypertension.

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