Type 2 Myocardial Infarction Caused by Orthostatic Hypotension With Post-transcatheter Aortic Valve Implantation: A Case Report.

This case report delineates the occurrence and management of type 2 myocardial infarction (MI) in an 89-year-old woman following transcatheter aortic valve implantation (TAVI). The patient, with a history of severe aortic stenosis, hypertension, dyslipidemia, and colorectal cancer, presented with nausea and significant hypotension. Initial assessments revealed elevated troponin levels, atrial fibrillation, and ST-segment depression, leading to a diagnosis of type 2 MI. This condition was attributed to the interplay between left ventricular hypertrophy, hypotension-induced dehydration, and increased myocardial oxygen demand. The patient with post-TAVI exhibited dynamic changes in cardiac hemodynamics, with improvements in left ventricular function but persistent hypertrophy and diastolic dysfunction. This state, combined with hypotension due to diuretic-induced dehydration and atrial fibrillation, precipitated a mismatch in myocardial oxygen supply and demand. The cessation of diuretics and initiation of rehydration therapy stabilized her condition, with subsequent normalization of troponin levels and blood pressure. This case highlights the complexity of managing type 2 MI in elderly patients post-TAVI. It underscores the importance of holistic consideration of both myocardial oxygen supply and demand factors, particularly in left ventricular hypertrophy and diastolic dysfunction. The multifactorial nature of type 2 MI necessitates a tailored approach to diagnosis and management, emphasizing the need for comprehensive post-procedural care in patients undergoing TAVI.

Role of KNDy Neurons Expressing Kisspeptin, Neurokinin B, and Dynorphin A as a GnRH Pulse Generator Controlling Mammalian Reproduction.

Increasing evidence accumulated during the past two decades has demonstrated that the then-novel kisspeptin, which was discovered in 2001, the known neuropeptides neurokinin B and dynorphin A, which were discovered in 1983 and 1979, respectively, and their G-protein-coupled receptors, serve as key molecules that control reproduction in mammals. The present review provides a brief historical background and a summary of our recent understanding of the roles of hypothalamic neurons expressing kisspeptin, neurokinin B, and dynorphin A, referred to as KNDy neurons, in the central mechanism underlying gonadotropin-releasing hormone (GnRH) pulse generation and subsequent tonic gonadotropin release that controls mammalian reproduction.

Central µ-Opioid Receptor Antagonism Blocks Glucoprivic LH Pulse Suppression and Gluconeogenesis/Feeding in Female Rats.

Energetic status often affects reproductive function, glucose homeostasis, and feeding in mammals. Malnutrition suppresses pulsatile release of the gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) and increases gluconeogenesis and feeding. The present study aims to examine whether ß-endorphin-µ-opioid receptor (MOR) signaling mediates the suppression of pulsatile GnRH/LH release and an increase in gluconeogenesis/feeding induced by malnutrition. Ovariectomized female rats treated with a negative feedback level of estradiol-17ß (OVX + low E2) receiving 2-deoxy-D-glucose (2DG), an inhibitor of glucose utilization, intravenously (iv) were used as a malnutrition model. An administration of D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP), a selective MOR antagonist, into the third ventricle blocked the suppression of the LH pulse and increase in gluconeogenesis/feeding induced by iv 2DG administration. Histological analysis revealed that arcuate Kiss1 (kisspeptin gene)-expressing cells and preoptic Gnrh1 (GnRH gene)-expressing cells co-expressed little Oprm1 (MOR gene), while around 10% of arcuate Slc17a6 (glutamatergic marker gene)-expressing cells co-expressed Oprm1. Further, the CTOP treatment decreased the number of fos-positive cells in the paraventricular nucleus (PVN) in OVX + low E2 rats treated with iv 2DG but failed to affect the number of arcuate fos-expressing Slc17a6-positive cells. Taken together, these results suggest that the central ß-endorphin-MOR signaling mediates the suppression of pulsatile LH release and that the ß-endorphin may indirectly suppress the arcuate kisspeptin neurons, a master regulator for GnRH/LH pulses during malnutrition. Furthermore, the current study suggests that central ß-endorphin-MOR signaling is also involved in gluconeogenesis and an increase in food intake by directly or indirectly acting on the PVN neurons during malnutrition in female rats.