Leptin is a 16-kDa-peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake and elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. While the relevance of endogenous leptin needs further clarification, it appears to function as a pressure and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular, and cardiac damage.

Adipose tissue should be regarded as a potentially important mediator of cardiorenal physiology. Further research awaits the characterization of additional mechanisms of action of leptin, including its interface with other important endocrine and hemodynamic sodium-volume regulatory systems, in both health and disease, particularly in obesity and related comorbidities. This information could lead to the development of leptin analogues as well as leptin receptor blockers that given specific circumstances could optimize the beneficial actions of the hormone and minimize its deleterious effects.

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Background: Spontaneous coronary artery dissection (SCAD) has been reported to be a rare cause of acute coronary syndrome and sudden cardiac death. The clinical presentation of SCAD varies from asymptomatic to sudden death. Pregnancy is associated with SCAD, and autoimmune diseases, especially systemic lupus erythematosus (SLE), may play an important role in SCAD etiology. Case Report: A 37-year-old female with hypertension, SLE, a history of preeclampsia with 3 cesarean deliveries, and an active smoking habit presented to the emergency department with chest pain. On arrival, the patient was hypertensive with blood pressure of 152/122 mm Hg and a normal heart rate and respiratory rate. Given the patient's history of SLE and preeclampsia, antiphospholipid antibodies were tested. The anti-β 2 -glycoprotein 1 immunoglobulin G concentration was elevated at 30 U/mL, and lupus anticoagulant was positive. Electrocardiogram showed minimum ST elevation in lead V2. Initial troponin was 0.1 ng/mL, with a peak of 54.5 ng/mL after 6 hours. Aspirin 325 mg was administered, and the patient underwent urgent cardiac catheterization. Intravascular angiography showed evidence of intimal flap (mid left anterior descending artery) spontaneous dissection with subintimal hematoma. The angioplasty resulted in successful stent placement in the mid left anterior descending artery. Conclusion: SCAD diagnosis is challenging and requires a high index of suspicion. This case shows the challenge of early diagnosis of SCAD and highlights its association with autoimmune diseases, specifically SLE. Early recognition of this pathology results in better outcomes.