Obesity cardiomyopathy
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]
Synonyms and keywords:
Overview
Obesity cardiomyopathy is defined as congestive heart failure due to structural and hemodynamic changes because of obesity. Increased total blood volume and cardiac output because of the high metabolic activity of excessive fat in long-standing obesity may lead to left ventricular dilation, increased left ventricular wall stress, compensatory left ventricular hypertrophy, and left ventricular diastolic dysfunction. Inadequate hypertrophy might tend to left ventricular systolic dysfunction due to high wall stress. .sleep apnea/ obesity hypoventilation syndrome might tend to pulmonary hypertension and subsequent right ventricular structural changes.
My references (Temporary)
Historical Perspective
Obesity cardiomyopathy is a new term, but the association between obesity and cardiac malfunction dates as far back as the late 1700s.
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"The initial mention of excess deposition of fat involving the heart of obese individuals was in 1783. About two decades later (in 1806), adipose tissue surrounding the heart in obese individuals was suspected to oppress the heart leading to sudden death [8]. In the late 19th Century [9,10] and in the early 20th Century [11] research evidence of the deleterious effect of obesity on cardiac function began to accumulate. However, the initial clinical descriptions of a pathologic obesity-associated cardiac morphology and dysfunction appeared in 1933. Saphir and Corrigan [12], and Smith and Willius [13] described the deleterious effect of fatty infiltration or adiposity of the heart on cardiac function and structure.
Since then, several subsequent studies have demonstrated cardiomyopathic processes caused by obesity may involve both the left and right sides of the heart, which occur in the absence of other cardiac or extra cardiac conditions associated with morbid obesity [14-18]. These conditions mainly include systemic hypertension, diabetes mellitus and coronary artery disease (CAD) but which on their own could contribute to cardiac decompensation, and as such, they remain significant risk factors accelerating the development of OCM [18-20]. More recently, the Framingham Heart Study (FHS) further reported obesity is an independent risk factor for the development of HF, demonstrating its deleterious effect on the ventricular function [21,22]. 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. 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.
Research on the prevalence of obesity in the general population has been extensive. However, a longitudinal systematic epidemiological study by Ng and associates [23] remains the biggest and most powerful. Spanning over three decades (1980-2013) and recruiting individuals aged between two (2) years and over 80 years old from 188 countries, the study reported the highest prevalence of obesity (defined as BMI ≥ 30 kg/m2) in Oceania, North Africa and the Middle East, which exceeded 50% of the general population. The prevalence was lower but still very high on other parts of the world. In North America, a third of the population was obese while in Western Europe, a fifth of the population was obese [23]. 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"
Classification
There is no established system for the classification of obesity cardiomyopathy.
This is a not for the author and will be edited:
"""" Obesity cardiomyopathy has been long recognized as a clinical entity but current morphological-and functional-based classification systems have excluded it as a distinct form of cardiomyopathy. The European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases [24] does not classify OCM as a type of cardiomyopathy. On the other hand, the 2016 Scientific Statement of the American Heart Association (AHA) classifies OCM as a sub-type of dilated cardiomyopathy (DM) under endocrine or metabolic etiologies of DCM [25]. In support of AHA’s classification, Kasper et al. [26] found a higher incidence of idiopathic DCM (77% versus 36%) among obese patients (mean body weight 130 kg) compared with lean patients (mean body weight 71kg). Several other studies have also demonstrated an association between obesity and idiopathic DCM [27-30] with some reporting a direct toxic effect of obesity on cardiac morphology and function [27,29,30].
Classification of OCM as a sub-type or an etiology of DCM adds to the current considerable debate to the existence of a true obesity-induced cardiomyopathy. Although OCM has been documented in rodent models, it is unclear whether isolated obesity can directly lead to cardiomyopathy in humans. Moreover, majorities of obese individuals have concomitant and likely synergistic risk factors for developing cardiac dysfunction, DCM and heart failure [27] [29,31]. 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."
Pathophysiology
It is thought that obesity cardiomyopathy is the result of hemodynamic changes and systemic metabolic changes of adeposity.
- An association between obesity and heart failure has been shown in epidemiological studies
- Clinical studies have shown the association between obesity and left ventricular dysfunction, independent of hypertension, coronary artery disease, and other heart diseases.
- Experimental studies demonstrated structural and functional changes in the myocardium in response to obesity.
The most important mechanisms in the development of obesity cardiomyopathy are:
- Metabolic disturbances (insulin resistance, increased free fatty acid levels, and also increased levels of adipokines),
- A metabolic disturbances (insulin resistance, increased free fatty acid levels, and also increased levels of adipokines),
- Activation of the renin-angiotensin-aldosterone and sympathetic nervous systems,
- Myocardial remodeling,
- Small-vessel disease (both microangiopathy and endothelial dysfunction).
| Mechanism | Effects/ Results |
| Hemodynamics | Increased blood volume |
| Increased stroke volume/Work | |
| Increased arterial pressure | |
| Increased LV wall stress | |
| Pulmonary artery hypertension | |
| Cardiac Structure | LV concentric remodeling |
| LV hypertrophy (eccentric/concentric) | |
| Left atrial enlargement | |
| RV hypertrophy | |
| Cardiac Function | LV diastolic dysfunction |
| LV systolic dysfunction | |
| RV failure | |
| Inflammation | Increased C-reactive protein |
| Over-expression of tumor necrosis factors (TNF) | |
| Neurohumoral | Insulin resistance and hyperinsulinemia |
| Leptin resistance and hyperleptinemia | |
| Reduced adiponectin | |
| Sympathetic nervous system over-activation | |
| Activation of renin-angiotensin-aldosterone system | |
| Cellular | Hypertrophy |
| Apoptosis | |
| Fibrosis |
Causes
Obesity cardiomyopathy may be caused by hemodynamic changes and systemic metabolic changes of adeposity.
Obesity itself and comorbidities of obesity such as hypertension, diabetes, dyslipidemia, atherosclerosis, chronic kidney disease, obstructive sleep apnea and subsequent pulmonary hypertension are all among causes of obesity cardiomyopathy.
Differentiating Obesity Cardiomyopathy from other Diseases
Obesity cardiomyopathy must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].
OR
obesity cardiomyopathy must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].
Epidemiology and Demographics
The incidence/prevalence of obesity cardiomyopathy is approximately [number range] per 100,000 individuals worldwide.
OR
In [year], the incidence/prevalence of obesity cardiomyopathy was estimated to be [number range] cases per 100,000 individuals worldwide.
OR
In [year], the incidence of obesity cardiomyopathy is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.
Patients of all age groups may develop obesity cardiomyopathy.
OR
The incidence of obesity cardiomyopathy increases with age; the median age at diagnosis is [#] years.
OR
obesity cardiomyopathy commonly affects individuals younger than/older than [number of years] years of age.
OR
[Chronic disease name] is usually first diagnosed among [age group].
OR
[Acute disease name] commonly affects [age group].
There is no racial predilection to obesity cardiomyopathy.
OR
obesity cardiomyopathy usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop obesity cardiomyopathy.
obesity cardiomyopathy affects men and women equally.
OR
[Gender 1] are more commonly affected by obesity cardiomyopathy than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.
The majority of obesity cardiomyopathy cases are reported in [geographical region].
OR
obesity cardiomyopathy is a common/rare disease that tends to affect [patient population 1] and [patient population 2].
besity is becoming a global epidemic,1,2 and in the past 10 years in the United States, dramatic increases in obesity have occurred in both children and adults.3
The prevalence of HF is 2-3% of the population in industrialized countries [2]. Approximately 5.7 million American adults have HF and require frequent hospitalizations [3]. ... Obesity-related cardiomyopathy is estimated to cause 11% of HF cases in males and up to 14% in women [
Risk Factors
There are no established risk factors for obesity cardiomyopathy.
OR
The most potent risk factor in the development of obesity cardiomyopathy is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].
OR
Common risk factors in the development of obesity cardiomyopathy include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
OR
Common risk factors in the development of obesity cardiomyopathy may be occupational, environmental, genetic, and viral.
. 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.
Screening
There is insufficient evidence to recommend routine screening for [disease/malignancy].
OR
According to the [guideline name], screening for obesity cardiomyopathy is not recommended.
OR
Almost every obese patient must be screened for obesity comorbidities which predispose them to the development of heart disease and obesity cardiomyopathy in particular. Screening in morbid obese patients should include diabetes, obstructive sleep apnea (OSA), hypertension, pump failure, etc. It should be noted that history and physical examination is not appropriate in certain scenarios like OSA. A basic echocardiographic study is warranted in morbidly obese patients, particularly those with comorbidities. [4]
According to the [guideline name], screening for obesity cardiomyopathy by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].
adiponectin has been proposed as a biomarker that might serve as a suitable screening test facilitating early intervention and prevention of heart failure (130, 275, 283).[5] . Several reports have suggested that leptin directly induced hypertrophy in both human and rodent cardiomyocytes. [6]
Natural History, Complications, and Prognosis
If left untreated, [#]% of patients with obesity cardiomyopathy may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
OR
Common complications of obesity cardiomyopathy include [complication 1], [complication 2], and [complication 3].
OR
Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with obesity cardiomyopathy is approximately [#]%.
Diagnosis
Diagnostic Study of Choice
The diagnosis of obesity cardiomyopathy is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].
OR
The diagnosis of obesity cardiomyopathy is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].
OR
The diagnosis of obesity cardiomyopathy is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].
OR
There are no established criteria for the diagnosis of obesity cardiomyopathy.
History and Symptoms
The majority of patients with obesity cardiomyopathy are asymptomatic.
OR
The hallmark of obesity cardiomyopathy is [finding]. A positive history of [finding 1] and [finding 2] is suggestive of obesity cardiomyopathy. The most common symptoms of obesity cardiomyopathy include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of obesity cardiomyopathy include [symptom 1], [symptom 2], and [symptom 3].
Physical Examination
Patients with obesity cardiomyopathy usually appear [general appearance]. Physical examination of patients with obesity cardiomyopathy is usually remarkable for [finding 1], [finding 2], and [finding 3].
OR
Common physical examination findings of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
OR
The presence of [finding(s)] on physical examination is diagnostic of obesity cardiomyopathy.
OR
The presence of [finding(s)] on physical examination is highly suggestive of obesity cardiomyopathy.
Laboratory Findings
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of obesity cardiomyopathy.
OR
Laboratory findings consistent with the diagnosis of obesity cardiomyopathy include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
OR
[Test] is usually normal among patients with obesity cardiomyopathy.
OR
Some patients with obesity cardiomyopathy may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
OR
There are no diagnostic laboratory findings associated with obesity cardiomyopathy.
Electrocardiogram
There are no ECG findings associated with obesity cardiomyopathy.
OR
An ECG may be helpful in the diagnosis of obesity cardiomyopathy. Findings on an ECG suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
It should be noted that "Although the QTc may not be extremely increased (≈440 ms) in the obese population, it is important to emphasize that screening for prolonged QT in obesity may have stringent criteria because a prolongation of QTc of >420 ms may be predictive of increased mortality rates in a healthy population followed up for 15 years." [8][9]
X-ray
There are no x-ray findings associated with obesity cardiomyopathy.
OR
An x-ray may be helpful in the diagnosis of obesity cardiomyopathy. Findings on an x-ray suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
OR
There are no x-ray findings associated with obesity cardiomyopathy. However, an x-ray may be helpful in the diagnosis of complications of obesity cardiomyopathy, which include [complication 1], [complication 2], and [complication 3].
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with obesity cardiomyopathy.
OR
Echocardiography/ultrasound may be helpful in the diagnosis of obesity cardiomyopathy. Findings on an echocardiography/ultrasound suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
OR
There are no echocardiography/ultrasound findings associated with obesity cardiomyopathy. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of obesity cardiomyopathy, which include [complication 1], [complication 2], and [complication 3].
CT scan
There are no CT scan findings associated with obesity cardiomyopathy.
OR
[Location] CT scan may be helpful in the diagnosis of obesity cardiomyopathy. Findings on CT scan suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
OR
There are no CT scan findings associated with obesity cardiomyopathy. However, a CT scan may be helpful in the diagnosis of complications of obesity cardiomyopathy, which include [complication 1], [complication 2], and [complication 3].
MRI
There are no MRI findings associated with obesity cardiomyopathy.
OR
[Location] MRI may be helpful in the diagnosis of obesity cardiomyopathy. Findings on MRI suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
OR
There are no MRI findings associated with obesity cardiomyopathy. However, a MRI may be helpful in the diagnosis of complications of obesity cardiomyopathy, which include [complication 1], [complication 2], and [complication 3].
Other Imaging Findings
There are no other imaging findings associated with obesity cardiomyopathy.
OR
[Imaging modality] may be helpful in the diagnosis of obesity cardiomyopathy. Findings on an [imaging modality] suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
There are no other diagnostic studies associated with obesity cardiomyopathy.
OR
[Diagnostic study] may be helpful in the diagnosis of obesity cardiomyopathy. Findings suggestive of/diagnostic of obesity cardiomyopathy include [finding 1], [finding 2], and [finding 3].
OR
Other diagnostic studies for obesity cardiomyopathy include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
There is no treatment for obesity cardiomyopathy; the mainstay of therapy is supportive care.
OR
Supportive therapy for obesity cardiomyopathy includes [therapy 1], [therapy 2], and [therapy 3].
OR
The majority of cases of obesity cardiomyopathy are self-limited and require only supportive care.
OR
obesity cardiomyopathy is a medical emergency and requires prompt treatment.
OR
The mainstay of treatment for obesity cardiomyopathy is [therapy].
OR The optimal therapy for [malignancy name] depends on the stage at diagnosis.
OR
[Therapy] is recommended among all patients who develop obesity cardiomyopathy.
OR
Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].
OR
Pharmacologic medical therapies for obesity cardiomyopathy include (either) [therapy 1], [therapy 2], and/or [therapy 3].
OR
Empiric therapy for obesity cardiomyopathy depends on [disease factor 1] and [disease factor 2].
OR
Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].
Surgery
Surgical intervention is not recommended for the management of obesity cardiomyopathy.
OR
Surgery is not the first-line treatment option for patients with obesity cardiomyopathy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]
OR
The mainstay of treatment for obesity cardiomyopathy is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].
OR
The feasibility of surgery depends on the stage of [malignancy] at diagnosis.
OR
Surgery is the mainstay of treatment for [disease or malignancy].
Primary Prevention
There are no established measures for the primary prevention of obesity cardiomyopathy.
OR
There are no available vaccines against obesity cardiomyopathy.
OR
Effective measures for the primary prevention of obesity cardiomyopathy include [measure1], [measure2], and [measure3].
OR
[Vaccine name] vaccine is recommended for [patient population] to prevent obesity cardiomyopathy. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].
Secondary Prevention
There are no established measures for the secondary prevention of obesity cardiomyopathy.
OR
Effective measures for the secondary prevention of obesity cardiomyopathy include [strategy 1], [strategy 2], and [strategy 3].
References
- ↑ 1.0 1.1 Ebong IA, Goff DC, Rodriguez CJ, Chen H, Bertoni AG (2014). "Mechanisms of heart failure in obesity". Obes Res Clin Pract. 8 (6): e540–8. doi:10.1016/j.orcp.2013.12.005. PMC 4250935. PMID 25434909.
- ↑ Wong C, Marwick TH (2007). "Obesity cardiomyopathy: pathogenesis and pathophysiology". Nat Clin Pract Cardiovasc Med. 4 (8): 436–43. doi:10.1038/ncpcardio0943. PMID 17653116.
- ↑ Alpert MA (2001). "Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome". Am J Med Sci. 321 (4): 225–36. doi:10.1097/00000441-200104000-00003. PMID 11307864.
- ↑ Robertson J, Schaufelberger M, Lindgren M, Adiels M, Schiöler L, Torén K; et al. (2019). "Higher Body Mass Index in Adolescence Predicts Cardiomyopathy Risk in Midlife". Circulation. 140 (2): 117–125. doi:10.1161/CIRCULATIONAHA.118.039132. PMC 6635044 Check
|pmc=value (help). PMID 31132859. - ↑ Patel DA, Srinivasan SR, Xu JH, Chen W, Berenson GS (2006). "Adiponectin and its correlates of cardiovascular risk in young adults: the Bogalusa Heart Study". Metabolism. 55 (11): 1551–7. doi:10.1016/j.metabol.2006.06.028. PMID 17046560.
- ↑ Madani S, De Girolamo S, Muñoz DM, Li RK, Sweeney G (2006). "Direct effects of leptin on size and extracellular matrix components of human pediatric ventricular myocytes". Cardiovasc Res. 69 (3): 716–25. doi:10.1016/j.cardiores.2005.11.022. PMID 16376323.
- ↑ Abel ED, Litwin SE, Sweeney G (2008). "Cardiac remodeling in obesity". Physiol Rev. 88 (2): 389–419. doi:10.1152/physrev.00017.2007. PMC 2915933. PMID 18391168.
- ↑ Schouten EG, Dekker JM, Meppelink P, Kok FJ, Vandenbroucke JP, Pool J (1991). "QT interval prolongation predicts cardiovascular mortality in an apparently healthy population". Circulation. 84 (4): 1516–23. doi:10.1161/01.cir.84.4.1516. PMID 1914093.
- ↑ Poirier P, Giles TD, Bray GA, Hong Y, Stern JS, Pi-Sunyer FX; et al. (2006). "Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism". Circulation. 113 (6): 898–918. doi:10.1161/CIRCULATIONAHA.106.171016. PMID 16380542.