RESUMO
BACKGROUND: Myocardial bridging is a common anatomical malformation, and the milking effect is a characteristic phenomenon of myocardial bridging in coronary angiography. Generally, the phenomenon is invariable. However, this article reports an inconceivably rare myocardial bridging phenomenon that breaks through our conventional views. The milking effect changed obviously in two coronary angiography examinations, which subverted the traditional deep-rooted view of the myocardial bridging phenomenon and revealed the limitations of coronary angiography in diagnosing myocardial bridging and judging the prognosis of it. CASE SUMMARY: A 63-year-old man was diagnosed with ST-segment elevation myocardial infarction and received primary percutaneous coronary intervention on December 26, 2019. His heart rate was 104 beats per minute, and blood pressure was 15.3/10.3 kPa. A severe milking effect was found in the left anterior descending coronary artery during his index coronary angiography on January 14, 2020. The patient was given intensive medical management, including a ß1-adrenergic receptor blocker, during hospitalization and after discharge. Unexpectedly, coronary angiography showed that the previous impressive milking effect was dramatically alleviated (close to normal) at the follow-up on October 13, 2020. At that moment, the patient's heart rate was 83 beats per minute, and blood pressure was 12.7/8.0 kPa. CONCLUSION: The myocardial bridging phenomenon is not invariable and, in certain circumstances, may vary. Furthermore, the autonomic nervous system may be involved in the myocardial bridging phenomenon.
RESUMO
Duraplasty is critical to the maintenance of anatomical integrity and the protection of brain tissue. Allotransplantation of cadaveric dura mater was abandoned after it was found to transmit Creutzfeldt-Jakob disease (CJD). In this study, the usefulness of a xenogeneic dura mater for dural reconstruction was tested. Twelve dogs were randomly assigned to 4 groups. To simulate the condition of patients with brain surface injury, an area of approximately 2 cm x 1.5 cm of the dura mater was removed to create a defect. Xenogeneic dura mater derived from porcine pericardium was trimmed to the shape and size of the defect and sutured to the endogenous dura mater. Muscles at the apex of the skull and scalp were also sutured. Three dogs were euthanized at 3, 6, 9, and 12 months after implantation and the xenogeneic dura mater and surrounding endogenous tissue were examined macroscopically and microscopically. Three months after implantation, the graft site had begun to heal. Macroscopically, at 6, 9, and 12 months after implantation, the graft had healed completely with the surrounding tissue. No boundary between the graft and surrounding tissue was distinguishable, and the two could not be separated. The graft was smoothly epithelialized and nonadherent to the brain surface. Microscopically, the inner surface of the implant was covered with epithelial cells, and internal capillaries, subepithelial fibrous tissue deposition, and fibroblast proliferation were observed. The xenogeneic dura mater progressively degraded over time. No cysts and no neutrophilic or lymphocytic inflammatory cell response developed between the implant and the recipient brain parenchyma. The modified xenogeneic dura mater is sufficiently biocompatible to allow epithelialization of its inner surface without adherence to brain tissue. No abnormalities develop in recipients, and the xenograft is gradually biodegraded and replaced by endogenous tissue identical to the endogenous dura mater.