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.
- 1783: The first mention of excess deposition of fat around the heart of obese individuals in novel literature.[3]
- 1806: Fat tissue surrounding the heart of obese subjects was suggested as the culprit of heart disease and sudden death in obese patients.[3]
- late 19th Century and the early 20th Century: Shreds of evidence of a deleterious effect of obesity on cardiac function has appeared in the published research.
- 1933: the initial clinical descriptions of a pathologic obesity-associated cardiac morphology and dysfunction suggested by Saphir and Corrigan, and Smith and Willius."ADIPOSITY OF THE HEART: A CLINICAL AND PATHOLOGIC STUDY OF ONE HUNDRED AND THIRTY-SIX OBESE PATIENTS | JAMA Internal Medicine | JAMA Network"."FATTY INFILTRATION OF THE MYOCARDIUM | JAMA Internal Medicine | JAMA Network".
- late 20th and early 21st Century: Plenty of published studies revealed the cardiomyopathic processes caused by obesity and suggested that it may involve both the left and right sides of the heart, and it could occur in the absence of other cardiac or extracardiac conditions associated with morbid obesity such as systemic hypertension, diabetes mellitus and coronary artery disease (CAD). [4][3]
- Framingham Heart Study: FHS reported obesity is an independent risk factor for the development of CHF.
- Nevertheless, there are some authors and scientists that believe there is no such a disease, and almost every obese patients with cardiomyopathy are suffering from another disease/comorbidity of obesity.[5]
- Obesity as a real disorder and worldwide problem:
- Ng and associates study: as of February 2020, their study remains the biggest and most powerful study in the epidemiology of obesity. For more than three decades (1980-2013), they recruited subjects aged between two and over 80 years old from 188 countries; the highest prevalence of obesity has been reported in Oceania, North Africa, and the Middle East, respectively which exceeded 50% of the general population. The prevalence was a little lower but still extremely high all around the world. Almost one-third of the population was obese in North America, while in Western Europe, twenty percent of the population was obese. This is a worldwide silent catastrophe.[6]
Classification
- There is no globally accepted established system for the classification of obesity cardiomyopathy.
- Although it has been defined as a clinical entity for many years, "current morphological-and functional-based classification systems have excluded it as a distinct form of cardiomyopathy."[7]
- American and European cardiology societies classification contradicts in this case:
- The European Society of Cardiology (ESC) does not classify obesity cardiomyopathy as a type of cardiomyopathy.
- The American Heart Association (AHA) classifies obesity cardiomyopathy as a sub-type of dilated cardiomyopathy under endocrine or metabolic etiologies of dilated cardiomyopathy.[8]
- The authors would like to support AHA’s classification. Nevertheless, the topic is still extremely controversial and needs further excavation.
- A higher incidence of idiopathic dilated cardiomyopathy has been reported among obese patients compared to their lean counterparts in many studies, some studies reported a direct toxic effect of obesity on cardiac morphology and function.
- There is no doubt that classification of obesity cardiomyopathy as a sub-type or an etiology of dilated cardiomyopathy might be immature. It is still controversial whether there is true obesity-induced cardiomyopathy or not? [9]
- Although obesity cardiomyopathy has been developed in obese rodent models, it is still unclear whether isolated obesity can directly lead to cardiomyopathy in humans, or so-called obesity cardiomyopathy is solely the result of comorbidities of obesity.
- Plenty of obese patients have a collection of concomitant and synergistic risk factors for developing cardiac dysfunction, dilated cardiomyopathy and heart failure.[10][2]
- Additionally, it is almost impossible to find a series of obese patients without hypertension, dyslipidemia, glucose intolerance and coronary artery diseases to study.
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:[11][8][4][3][2][1]
- 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). [1]
| 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 adiposity.
- 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. [11][9][7][4][3][2][1]
Differentiating Obesity Cardiomyopathy from other Diseases
Obesity cardiomyopathy must be differentiated from other diseases that cause cardiomyopathy, such as hypertension (HTN), ischemic heart disease (IHD), pulmonary arterial hypertension (PAH), and obstructive sleep apnea (OSA).[12][7][5][3][2][1]
Epidemiology and Demographics
- Ng and associates study: as of February 2020, their study remains the biggest and most powerful study in the epidemiology of obesity. For more than three decades (1980-2013), they recruited subjects aged between two and over 80 years old from 188 countries; the highest prevalence of obesity has been reported in Oceania, North Africa, and the Middle East, respectively which exceeded 50% of the general population. The prevalence was a little lower but still extremely high all around the world. Almost one-third of the population was obese in North America, while in Western Europe, twenty percent of the population was obese. This is a worldwide silent catastrophe.[6]
- The prevalence of congestive heart failure (CHF) is approximately 2000-3000 per 100,000 individuals in industrialized countries. Around 5.7 million American adults need frequent hospitalization due to heart failure.[9][4][3][2][1]
- Obesity cardiomyopathy is estimated to be responsible for 11% of heart failure cases in males and around 14% in women.[3][2][1]
Risk Factors
- In morbidly obese patients, cardiomyopathy may result from obesity, which may be potentiated with an 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.[1][7][4][2]
Screening
- 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. [10][2]
- 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).[13] . Several reports have suggested that leptin directly induced hypertrophy in both human and rodent cardiomyocytes. [11] [12]
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." [14][15]
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
The mainstay of treatment for obesity cardiomyopathy is weight loss an control of comorbidities of obesity such as hypertension and obstructive sleep apnea.
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 1.2 1.3 1.4 1.5 1.6 1.7 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.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 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.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 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.
- ↑ 4.0 4.1 4.2 4.3 4.4 Alexander JK (1985). "The cardiomyopathy of obesity". Prog Cardiovasc Dis. 27 (5): 325–34. doi:10.1016/s0033-0620(85)80002-5. PMID 3975428.
- ↑ 5.0 5.1 Wilson PW, D'Agostino RB, Sullivan L, Parise H, Kannel WB (2002). "Overweight and obesity as determinants of cardiovascular risk: the Framingham experience". Arch Intern Med. 162 (16): 1867–72. doi:10.1001/archinte.162.16.1867. PMID 12196085.
- ↑ 6.0 6.1 Ng M, Fleming T, Robinson M, Thomson B, Graetz N, Margono C; et al. (2014). "Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013". Lancet. 384 (9945): 766–81. doi:10.1016/S0140-6736(14)60460-8. PMC 4624264. PMID 24880830.
- ↑ 7.0 7.1 7.2 7.3 Pinto YM, Elliott PM, Arbustini E, Adler Y, Anastasakis A, Böhm M; et al. (2016). "Proposal for a revised definition of dilated cardiomyopathy, hypokinetic non-dilated cardiomyopathy, and its implications for clinical practice: a position statement of the ESC working group on myocardial and pericardial diseases". Eur Heart J. 37 (23): 1850–8. doi:10.1093/eurheartj/ehv727. PMID 26792875.
- ↑ 8.0 8.1 Bozkurt B, Colvin M, Cook J, Cooper LT, Deswal A, Fonarow GC; et al. (2016). "Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association". Circulation. 134 (23): e579–e646. doi:10.1161/CIR.0000000000000455. PMID 27832612.
- ↑ 9.0 9.1 9.2 Goldberg IJ, Trent CM, Schulze PC (2012). "Lipid metabolism and toxicity in the heart". Cell Metab. 15 (6): 805–12. doi:10.1016/j.cmet.2012.04.006. PMC 3387529. PMID 22682221.
- ↑ 10.0 10.1 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. - ↑ 11.0 11.1 11.2 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.
- ↑ 12.0 12.1 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.
- ↑ 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.
- ↑ 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.