OVERVIEW
Obesity is a common group of metabolic disorders. Obesity is defined as weight over 20% of ideal body weight, over 20% to 40% of ideal body weight for mild obesity, over 40% to l00% of ideal body weight for moderate, over 100% of ideal body weight for severe, or over-obesity. The cardiac dysfunction caused by over-obesity is called obesity cardiomyopathy. 1933 Smith and Willius first reported congestive heart failure in over-obese patients without coronary artery disease, hypertension, valvular disease or other heart disease, and proposed the relationship between obesity and cardiac dysfunction.
Mildly and moderately obese patients generally do not show signs of circulatory stasis, although ventricular hypertrophy can occur. Patients with obesity cardiomyopathy can have a long asymptomatic period, and the earliest and most common symptoms are postexercise dyspnea and telangiectasia. These symptoms are episodic in nature and are due to impaired diastolic function. Patients with increased cardiac output and normal cardiac systolic function can have worsening symptoms with recent weight gain. If cardiac systolic function is normal at the time of the first episode, these symptoms may recur and worsen over a period of 10 to 15 years, and the patient’s cardiac systolic function may remain relatively good for a long period of time.
Etiology
When the body takes in more calories than it burns, the excess calories can be stored in the body as fat. When a considerable amount of storage is reached, obesity develops. Excessive obesity can cause cardiac dysfunction and develop into obesity cardiomyopathy.
Symptoms
1. Symptoms
Although mild and moderate obesity patients may have ventricular hypertrophy, they generally do not have the symptom of circulatory stasis. Obese cardiomyopathy patients can have a long asymptomatic period, the earliest and most common symptom is dyspnea after exercise, sitting breathing. These symptoms are episodic in nature and are due to impaired diastolic function. Patients with increased cardiac output and normal cardiac systolic function can have worsening symptoms with recent weight gain. If cardiac systolic function is normal at the time of the first episode, these symptoms may recur and worsen over a period of 10 to 15 years, and the patient’s cardiac systolic function may remain relatively good for a long period of time. Conversely, if cardiac decompensation is present, the prognosis is generally poor, but the course of the disease is not well understood. Some patients have apnea/hypopnea syndrome, in which, in addition to the symptoms of congestion of the physical and pulmonary circulation, there may be lethargy, depression, and disorientation due to CNS edema. Coma is rare and sudden death is common. In the presence of right heart insufficiency, epigastric discomfort and abdominal distension may occur.
2. Physical signs
Cardiac auscultation in patients with heart failure sometimes reveals systolic fourth heart sound, third heart sound, and hyperactive second heart sound of pulmonary valve. Although the jugular vein is filled, it is often difficult to observe. Twisting fine wet rales are often heard in the lungs. Hepatomegaly, ascites, and non-sunken edema of both lower extremities may be present in almost every overweight individual. Those with apnea/hypopnea syndrome may have cyanosis, and episodes of dyspnea are common, as well as conjunctival congestion, retinal congestion, and optic disc edema.
Examination
1. Laboratory examination
Laboratory examination of hypoxemia, often accompanied by respiratory acidosis, but with the improvement of circulatory stasis, there can be a certain degree of improvement.
2. Auxiliary examination
(1) Electrocardiogram (ECG): left deviation of the electrical axis, or right deviation with pulmonary P waves and low voltage. Patients with recurrent episodes of circulatory congestion may have atrial fibrillation, atrial flutter and various conduction blocks, with fatty infiltration of the conduction system and left atrial enlargement as the pathologic basis. Those patients with apnea/hypopnea syndrome may have sinus node lesions such as sinus arrest and sinus node efferent block.
(2) Chest X-ray Chest radiographs can be normal in obesity cardiomyopathy and most often show an enlarged heart with pulmonary bruits.
(3) Echocardiography In 80% to 98% of patients with obesity cardiomyopathy, the major structures can be visualized by transthoracic color Doppler echocardiography (TTE), and a complete TTE can be performed in 70% of patients. Because the heart is positioned differently than normal in the chest cavity and is somewhat “upturned,” the acoustic window for TTE is different than normal and the subxiphoid ultrasound image is not ideal. In about half of the patients, it is not possible to visualize the endocardial surface or to measure the ejection fraction. Transesophageal echocardiography (TEE) should compensate for the shortcomings of TTE, but the use of TEE in overweight patients has not been reported. Patients have increased left ventricular filling pressures. It has been studied with Doppler ultrasound that obese patients with normal blood pressure have a prolonged time to halving of overt mitral inflow pressure and a higher peak left ventricular filling velocity than controls in non-obese hypertensive patients or normals. The right ventricle is enlarged and hypertrophied in some patients, and right ventricular systolic function has been less well studied. Reduced right ventricular function and ejection fraction of 8% to 22% have been reported in obese patients.
Diagnosis
Obesity cardiomyopathy can be considered when progressive shortness of breath, telangiectasia and lower extremity edema occur in severely obese patients, and when X-ray chest radiographs show cardiac enlargement and pulmonary bruising. The following diagnostic criteria can be referred to.
Diagnostic criteria: ① extremely obese patients; ② heart enlargement (left ventricle is more obvious), may have congestive heart failure; ③ left ventricular end-diastolic pressure is close to the upper limit of the normal value at rest, and often rises when exercising; ④ with the significant decline in body weight, the above performance improves.
Differential Diagnosis
Differential diagnosis of obesity
Primary endocrine changes
Hypothalamic-pituitary
Possibly hereditary
Hyperinsulinemia
Hypothalamic or pituitary sexual tumors or
Sexually naive-pigmented retina-multiple
inflammatory lesions
Finger (toe) syndrome
Glucagon-like hormone excess
Brain tumor or surgical injury
Alsteom syndrome
Primary hypogonadism
Pseudotumor cerebri
Pseudohypoparathyroidism
Primary hypothyroidism
Empty ssella syndrome
Down syndrome
Polycystic ovary syndrome
Familial obesity
Treatment of obesity
1. Weight reduction
It is the most effective long-term treatment option for obesity cardiomyopathy. With effective weight loss, many cardiac structural abnormalities and hemodynamics can be significantly improved, and blood pressure can be reduced to lower levels. If maintained for 1 to 3 years, all obese patients seem to have lower systolic and diastolic blood pressure. As weight decreases, patients’ blood volume, cardiac output, and body oxygen consumption decrease, and cardiac output and body oxygen consumption during exercise are also lower than before weight loss. However, heart rate, left ventricular end-diastolic pressure, pulmonary vascular wedge pressure, body circulation vascular resistance, and pulmonary artery pressure do not decrease at rest and during exercise after weight loss.
Measures such as low-calorie, low-salt-restricted diets and appropriate exercise should be taken, and long-term adherence can lead to gradual weight loss. Starvation dietary restriction is as effective, but dangerous, generally not used, severe low-calorie and low-sodium dietary restriction and starvation dietary restriction can cause sodium diuresis and blood volume reduction, resulting in a decrease in sympathetic activity, which can lead to postural hypotension, dizziness, and even fainting in patients whose blood pressure is originally normal.
2. Symptomatic treatment
(1) Control of heart failure When patients with obesity cardiomyopathy develop acute congestive heart failure, or severe pulmonary and circulatory stasis, the application of diuretics and the administration of oxygen are the urgent treatments. Digitalis preparations are available. There is limited experience with the application of vasodilators. Acute management should also include low salt and dietary restriction.
(2) Control of heart rate If rapid atrial fibrillation or atrial flutter is present, digitalis preparations can be used to control the ventricular rate. It should be emphasized that the patient’s serum digitalis level is related to the patient’s muscle rather than excess weight. Care should be taken to monitor blood potassium levels to prevent digitalis toxicity. Depending on the state of left heart function, consider whether to add beta-blockers or verapamil.
(3) Control of severe hypertension Beneficial for improving left ventricular function in hypertensive obese patients.
(4) Anticoagulant therapy Venous thrombosis and pulmonary embolism have a certain incidence, for those patients without contraindications, prophylactic application of heparin therapy has not yet been studied to confirm its efficacy.