Background: Sheehan syndrome, a type of hypopituitarism ensuing from postpartum hemorrhage, seldom manifests concomitantly with coronary atherosclerotic heart disease. The gestational period witnesses an augmentation in the pituitary gland's size, thereby escalating its oxygen requirements and rendering it more susceptible to hypoxic conditions. An acute, substantial hemorrhage during childbirth can precipitate ischemic necrosis in the anterior pituitary cells. This results in a marked decline in the secretion of its array of hormones, culminating in the degeneration of their respective target organs and the onset of multifarious symptomatic manifestations. Case presentation: We delineate two distinct cases of Sheehan syndrome conjoined with coronary atherosclerotic heart disease. In the first case, the patient, having a medical background of postpartum hemorrhage and percutaneous coronary intervention, presented with precordial and dorsal pain. Laboratory investigations indicated aberrantly elevated myocardial damage markers. Acute coronary syndrome was diagnosed upon admission. Further assessments, comprising pituitary hormone levels and MRI, unveiled pituitary atrophy (termed as "empty sella"), attenuated thyroid-stimulating hormone, and adrenocorticotropic hormone levels. A conclusive diagnosis of Sheehan syndrome was then ascertained. Following a regimen of hormone replacement therapy, the patient's physiological state attained stability. The second case involved a patient previously diagnosed with Sheehan syndrome, who exhibited symptoms such as chest constriction, dorsal discomfort, and transient syncope-induced fatigue. Acute coronary syndrome was diagnosed upon her admission. A subsequent comprehensive assessment, encompassing coronary angiography and cardiac MRI, revealed her afflictions to be variant angina pectoris and acquired QT prolongation syndrome. A subsequent course of hormone replacement therapy stabilized the patient's condition. Conclusion: Hypopituitarism, resulting from Sheehan syndrome, compromises central hormonal secretion, and the concomitant deficiency of multiple pituitary hormones can often obscure clinical manifestations, leading to potential diagnostic oversight. The resultant hypothyroidism can induce rhabdomyolysis, which could erroneously be diagnosed as an acute myocardial infarction and may predispose individuals to a spectrum of cardiovascular pathologies.