Unveiling Obesity-Related Cardiomyopathy: Scientific Weight Loss is the Core Solution for Cardiac Rehabilitation

Obesity-related cardiomyopathy: As early as 1933, Smith and Winius performed autopsies on 135 obese deceased individuals, reporting on four cases of significantly obese individuals who died of heart failure. No evidence of hypertension or other cardiac diseases was found during the autopsies. Based on this, the idea that obesity could cause cardiac dysfunction was first proposed. Later, it was reported that excessive obesity could lead to cardiomyopathy; therefore, the cardiac dysfunction caused by obesity was named "obesity-related cardiomyopathy."

I. Cardiac pathological manifestations of obesity-related cardiomyopathy

1. Increased cardiac weight with left ventricular hypertrophy
Smith and Winius found that within a weight range of 105 kg, cardiac weight was linearly correlated with body weight. Beyond this range, the heart/body weight ratio tended to decrease. Nevertheless, the average heart weight of obese individuals was 150 g heavier than that of non-obese individuals, and in some cases, the heart of an excessively obese patient could be 2-3 times larger than that of a non-obese individual of the same height. The most characteristic pathological change is eccentric hypertrophy of the left ventricle, occasionally with right ventricular hypertrophy.

2. Fatty Infiltration Autopsy revealed extensive fatty infiltration in the coronary artery distribution areas at the base of the heart, the atrioventricular groove, the base of the great vessels, and the surface of the right ventricle.

II. Mechanisms of Cardiomyopathy Caused by Obesity

(1) Extensive cardiac fatty infiltration can affect cardiac activity and myocardial nutrition, leading to ventricular dysfunction and even heart failure. Saphir and Corgan later reported two cases of sudden death in obese patients. One of them had significant arrhythmias before death. It is speculated that excessively obese patients, without other heart diseases, may experience various types of arrhythmias or even sudden death due to fatty infiltration of the sinoatrial node and atrioventricular bundle, usually with conduction system disorders being more pronounced.

(2) Changes in hemodynamics overload the heart. In obese patients, when exceeding standard weight, the increase in overall blood volume is positively correlated with weight gain, mainly due to an increase in the vascular bed. This increase in blood volume is consistent with an increase in resting cardiac output. Currently, inert gas flushing is used to estimate the blood flow in the fat deposit. Preliminary estimates suggest that, at rest, the average blood volume in obese individuals is 2–3 ml/min/100g of adipose tissue. Clearly, the high blood output in obese individuals is caused by the blood flow requirements of adipose tissue. ① Due to increased blood volume, left ventricular compliance decreases, and diastolic function declines, but left ventricular systolic function remains preserved, resulting in symptoms and signs of pulmonary and systemic vascular congestion. ② Long-term blood volume increases exceeding cardiac load, leading to increased cardiac output, which can cause myocardial hypertrophy regardless of the presence of hypertension. The ratio of myocardial wall thickness to cardiac chamber radius decreases, increasing ventricular wall tension and potentially causing left ventricular systolic dysfunction. Therefore, diastolic ventricular dysfunction occurs first, followed by systolic ventricular dysfunction; the distinction between the two relies primarily on ultrasound, radionuclide, and angiography.

III. Treatment All pathophysiological changes in obese cardiomyopathy patients are closely related to weight gain; therefore, weight reduction is key to treatment.

Clinical observations indicate that hemodynamic disturbances in obese individuals typically improve significantly with weight loss. As body weight decreases, overall blood volume and cardiac preload decrease accordingly, and cardiac output and oxygen consumption tend to return to normal.

Fasting is generally not used to reduce weight because it can cause potassium depletion in the myocardium, easily leading to ventricular fibrillation. It can also cause lactic acidosis, weakening myocardial contractility. Strict calorie restriction can cause severe hyponatremia and a decrease in blood volume, resulting in reduced sympathetic nerve activity, leading to orthostatic hypotension, dizziness, or even syncope.

For patients with other symptoms and complications, symptomatic treatment should be given.

Obstructive Sleep Apnea Syndrome: This syndrome refers to a series of symptoms caused by alveolar hypoxia in extremely obese patients without primary heart or lung disease, such as dyspnea, heart failure, and drowsiness. Weight loss can significantly improve clinical symptoms. Sleep apnea syndrome is more common in middle-aged and older adults. The incidence rate in people aged 30-69 is 0.7%-9%, with an average age of 48.7 years and a male-to-female ratio of 5.4:1. Obstructive respiratory syndrome causes severe inadequate ventilation, leading to a gradual increase in pulmonary artery pressure and pulmonary capillary pressure, a decrease in arterial oxygen partial pressure, and an increase in carbon dioxide partial pressure, which in turn causes a series of clinical manifestations such as decreased cardiac function and abnormalities of the central nervous system.