Inhibitory action of B-type natriuretic peptide on adrenocorticotropic hormone in patients with acute coronary syndrome.

In addition to the classical actions of hemodynamic regulation, natriuretic peptides (NPs) interact with various neurohumoral factors that are deeply involved in the pathophysiology of cardiovascular diseases. However, their effects on the hypothalamic-pituitary-adrenal (HPA) axis, which is activated under acute high-stress conditions in acute coronary syndrome (ACS), remain largely unknown. We investigated the impact of plasma B-type NP (BNP) on plasma adrenocorticotropic hormone (ACTH)-cortisol levels during the acute phase of ACS ischemic attacks. The study population included 436 consecutive patients with ACS for whom data were collected during emergency cardiac catheterization. Among them, biochemical data after acute-phase treatment were available in 320 cases, defined as the ACS-remission phase (ACS-rem). Multiple regression analyses revealed that plasma BNP levels were significantly negatively associated with plasma ACTH levels only during ACS attacks (P < 0.001), but not in ACS-rem, whereas plasma BNP levels were not significantly associated with plasma cortisol levels at any point. Accordingly, covariance structure analyses were performed to clarify the direct contribution of BNP to ACTH by excluding other confounding factors, confirming that BNP level was negatively correlated with ACTH level only during ACS attacks (ß = -0.152, P = 0.002), whereas BNP did not significantly affect ACTH in ACS-rem. In conclusion, despite the lack of a significant direct association with cortisol levels, BNP negatively regulated ACTH levels during the acute phase of an ACS attack in which the HPA axis ought to be activated. NP may alleviate the acute stress response induced by severe ischemic attacks in patients with ACS.NEW & NOTEWORTHY BNP negatively regulates ACTH during a severe ischemic attack of ACS in which hypothalamic-pituitary-adrenal axis ought to be activated, indicating an important role of natriuretic peptides as a mechanism of adaptation to acute critical stress conditions in humans.

A case of cardiac calcified amorphous tumor complicated with acute myocardial infarction.

An 80-year-old woman with a history of eosinophilic granulomatosis with polyangiitis, cardiac hypertrophy, and diabetes called for an ambulance after developing chest pain. She was diagnosed with acute myocardial infarction (AMI), and coronary angiography revealed occlusion of the right coronary artery. Coronary aspiration was performed, and coronary aspirate was white with calcified factor. After percutaneous coronary intervention, transthoracic echocardiography performed on day 25 revealed a hyperechoic mobile mass originating from the anterior mitral leaflet. As a mobile or rapidly increasing mass carries a high risk of embolism, we decided to perform surgical resection. Preoperative cerebral magnetic resonance imaging showed asymptomatic cerebral infarction, suggesting embolism by the cardiac mass. Resection of the cardiac mass was performed by cardiac surgeons. Microscopic pathology of cardiac mass revealed nodules of calcification and fibroblasts, leading to diagnosis of calcified amorphous tumor (CAT). Furthermore, the microscopic pathology of the coronary aspirate showed calcification, fibrin, and vascular endothelial cells. The pathological similarity of the cardiac mass and coronary aspirate indicated that the AMI has been caused by CAT. CAT causes systemic embolization; however, only 1 case of MI caused by CAT has been reported. We therefore experienced a rare case in which CAT caused AMI. .

Out-of-Hospital Cardiac Arrest Does Not Affect Post-Discharge Survival in Patients With Acute Myocardial Infarction.

Background: Acute myocardial infarction (AMI) patients complicated by out-of-hospital cardiac arrest (OHCA) show poor in-hospital outcomes. However, the post-discharge outcomes of survivors of OHCA have not been well studied. Methods and Results: Data for patients admitted to The Jikei University Kashiwa Hospital with AMI between April 2012 and March 2020 were examined retrospectively. The Jikei University Kashiwa Hospital is a tertiary emergency medical facility, so the frequency of OHCA in this hospital is higher than in an ordinary AMI population. Of 803 patients, 92 (11.5%) were complicated by OHCA. Of the 92 OHCA patients, 37 died in hospital, compared with 45 of 711 non-OHCA patients who died in hospital (P<0.001). OHCA was more frequent in men than in women. The estimated glomerular filtration rate was lower in those with than without OHCA. Long-term mortality was evaluated in patients discharged alive and followed-up at an outpatient clinic (n=635; median follow-up period 607 days). The long-term post-discharge mortality was comparable between AMI patients with and without OHCA. Conclusions: The post-discharge mortality of AMI patients with OHCA was comparable that of patients without OHCA.

Therapeutic hypothermia after cardiac arrest increases the plasma level of B-type natriuretic peptide.

Natriuretic peptides (NPs) regulate blood pressure and fluid homeostasis and exert various effects on the cardiovascular system. Recently, the relationship between NPs and the energy metabolism has been reported, and using a cell culture experiment system, we previously showed that NP activated brown cells in a low temperature environment while also suppressing a decrease in the cell temperature. However, few reports have described the secretion of NPs in cold environments, and there have been almost no studies of B-type natriuretic peptide (BNP) in humans. We investigated how NPs respond to cold environments in 21 patients who underwent therapeutic hypothermia (TH) after cardiac arrest. The plasma BNP levels were significantly increased (more than fivefold) during TH (logarithmically from 1.98 ± 0.79 to 2.63 ± 0.59, P < 0.01). During TH, diastolic pulmonary artery pressure (PAP) significantly decreased, and there were no significant changes in the stroke volume index (SVI). This increase of BNP was not associated with any hemodynamic changes. In contrast to our findings for BNP, the change in A-type NP (ANP) was quite small. We detected a significant increase in the plasma BNP levels during TH, unrelated to hemodynamics. This elevation of BNP levels seems to be potential influenced by hypothermia.

Coronary artery disease concomitant with immunoglobulin G4-related disease: a case report and literature review.

BACKGROUND: Immunoglobulin G4-related disease (IgG4-RD) is an autoimmune condition associated with high serum IgG4 levels which was first reported as autoimmune pancreatitis in 2001. Since then, many additional organs, such as bile duct, salivary gland, retroperitoneal organs, and liver, have been reported with high serum IgG4 levels in cases of IgG4-RD. However, evidence of the relationship between IgG4-RD and coronary artery disease (CAD) has been scare. Here, we report a case of CAD concomitant with IgG4-RD. CASE SUMMARY: A 74-year-old man was referred to our hospital with a chief complaint of chest pain and was admitted. The patient was found to have had a myocardial infarction with ST-segment elevation and underwent an emergent percutaneous coronary intervention. Owing to a rapidly increased blood glucose level, computed tomography was performed and showed autoimmune pancreatitis. An elevated serum level of IgG4 led to a diagnosis of IgG4-RD involving acute coronary syndrome (ACS). DISCUSSION: Cardiac involvement in IgG4-RD has been reported; however, cases of ACS concomitant with IgG4-RD are rare. Our report suggests that CAD, specifically ACS, can coexist in patients with IgG4-RD. Therefore, cases of concomitant CAD and IgG4-RD should be accurately diagnosed and evidence should be collected to elucidate the mechanism and characteristics of this condition.