Constrictive Pericarditis With Massive Calcification in Systemic Sclerosis Treated With Pericardiectomy: A Case Report.

Calcific constrictive pericarditis is a very rare complication of systemic sclerosis. This is the first report of surgically treated calcific constrictive pericarditis in systemic sclerosis. A 53 years-old woman, affected by limited systemic sclerosis, had a diagnosis of calcific constrictive pericarditis. She had a medical history of congestive heart failure since 2022. The patient was treated with pericardiectomy. Via a median sternotomy, the pericardium was dissected and removed from the midline to the left phrenic nerve, thus freeing the heart. Three months after the pericardiectomy, there was a significant clinical improvement. The calcific evolution of chronic pericarditis is a rare complication of systemic sclerosis. This case represents, at best of our knowledge, the first report of calcific constrictive pericarditis, in systemic sclerosis, treated with pericardiectomy.

Combined Treatment With Carotid Endoarterectomy and Coronary Artery Bypass Grafting: A Single-Institutional Experience in 222 Patients.

INTRODUCTION: Carotid atherosclerotic disease is a known independent risk factor of post operative stroke after coronary artery bypass grafting (CABG). The best management of concomitant coronary artery disease and carotid artery disease remains debated. Current strategies include simultaneous carotid endoarterectomy (CEA) and CABG, staged CEA followed by CABG, staged CABG followed by CEA, staged transfemoral carotid artery stenting (TF-CAS) followed by CABG, simultaneous TF-CAS and CABG and transcarotid artery stenting. METHODS: We report our experience based on a cohort of 222 patients undergoing combined CEA and CABG surgery who come to our observation from 2004 to 2020. All patients with >70% carotid stenosis and severe multivessel or common truncal coronary artery disease underwent combined CEA and CABG surgery at our instituion. 30% of patients had previously remote neurological symptoms or a cerebral CT-scan with ischemic lesions. Patients with carotid stenosis >70%, either asymptomatic or symptomatic, underwent CT-scan without contrast media to assess ischemic brain injury, and in some cases, if necessary, CT-angiography of the neck and intracranial vessels. RESULTS: The overall perioperative mortality rate was 4.1% (9/222 patients). Two patients (.9%) had periprocedural ipsilateral transient ischemic attack (TIA) which completely resolved by the second postoperative day. Two patients (.9%) had an ipsilateral stroke, while 7 patients (3.2%) had a stroke of the controlateral brain hemisphere. Two patients (.9%) patients were affected by periprocedural coma caused by cerebral hypoperfusion due to perioperative heart failure. There were no statistically significant differences between patients in Extracorporeal Circulation (ECC) and Off-pump patients in the onset of perioperative stroke. CONCLUSION: Our experience reported that combined surgical treatment of CEA and CABG, possibly Off-Pump, is a feasible treatment procedure, able to minimize the risk of post-operative stroke and cognitive deficits.

Effects of Sodium-Glucose Transporter 2 Inhibitors (SGLT2-I) in Patients With Ischemic Heart Disease (IHD) Treated by Coronary Artery Bypass Grafting via MiECC: Inflammatory Burden, and Clinical Outcomes at 5 Years of Follow-Up.

Introduction: Minimally invasive extracorporeal circulation (MiECC) reduced inflammatory burden, leading to best clinical outcomes in patients treated with coronary artery bypass grafting (CABG). Despite this, the patients with type 2 diabetes mellitus (T2DM) vs those without T2DM (non-T2DM) have a worse prognosis, caused by over-inflammation and modulated by sodium-glucose transporter 2 receptors. However, we evaluated the inflammatory burden and clinical outcomes in non-T2DM vs T2DM patients under sodium-glucose transporter 2 inhibitors (SGLT2-I users) vs non-SGLT2-I users at 5 years of follow-up post-CABG via MiECC. Materials and methods: In a multicenter study, we screened consecutive patients with indications to receive CABG. The study endpoints were the inflammatory burden (circulating serum levels of tumor necrosis factor-alpha (TNF-α), interleukin 1 and 6 (IL-1 and IL-6), C-reactive protein (CRP), and leucocytes count) and the clinical outcomes at follow-up of 5 years in non-T2DM vs SGLT2-I users, in non-T2DM vs non-SGLT2-I users, and SGLT2-I users vs non-SGLT2-I users. Results: At baseline, and at one year and 5 years of follow-up, the non-T2DM vs SGLT2-I users, non-T2DM vs non-SGLT2-I users, and SGLT2-I users vs non-SGLT2-I users had the lowest values of IL-1, IL-6, and TNF-α (p < 0.05). At one year of follow-up, SGLT2-I users vs non-T2DM and non-SGLT2-I users vs non-T2DM users had a higher rate of all deaths, cardiac deaths, re-myocardial infarction, repeat revascularization, and stroke, and of the composite endpoint (p < 0.05). In a multivariate Cox regression analysis, the composite endpoint was predicted by IL-1 [2.068 (1.367-3.129)], TNF-α [1.989 (1.081-2.998)], and SGLT2-I [0.504 (0.078-0.861)]. Conclusion: In T2DM patients, the SGLT2-I significantly reduced the inflammatory burden and ameliorated clinical outcomes at 5 years of follow-up post-CABG via MiECC.

Atherosclerotic Plaque Fissuration and Clinical Outcomes in Pre-Diabetics vs. Normoglycemics Patients Affected by Asymptomatic Significant Carotid Artery Stenosis at 2 Years of Follow-Up: Role of microRNAs Modulation: The ATIMIR Study.

Atherosclerotic plaque instability and rupture in patients with asymptomatic carotid artery stenosis (ACAS) is a leading cause of major adverse cardiac events (MACE). This could be mainly evidenced in patients with pre-diabetes. Indeed, the altered glucose homeostasis and insulin resistance could cause over-inflammation of atherosclerotic plaque, favoring its conversion to unstable phenotype with rupture and MACE. Notably, metformin therapy reducing the metabolic distress and the inflammatory burden could reduce MACE in ACAS patients with pre-diabetes. In this setting, the microRNAs (miRs) could be used as molecular biomarkers of atherosclerosis progression, plaque rupture, and worse prognosis in normoglycemics (NG) versus pre-diabetics metformin users (PDMU) versus pre-diabetics non-metformin users (PDNMU). However, our study aimed to investigate a wide miRNA panel in peripheral blood exosomes from patients with ACAS divided in NG versus PDMU versus PDNMU, and to associate the circulating miRNA expression profiles with MACE at 2 years of follow-up after endarterectomy. The study included 234 patients with ACAS divided into NG (n = 125), PDNMU (n = 73), and PDMU (n = 36). The miRs' expression profiles of circulating exosomes were determined at baseline and at 2 years of follow-up by Affymetrix microarrays from the patients' plasma samples from any study cohort. Then we collected and analyzed MACE at 2 years of follow-up in NG versus PDMU versus PDNMU. Prediabetics versus NG had over-inflammation (p < 0.05) and over expressed miR-24 and miR-27 at baseline. At 2 years of follow-up, PDNMU versus NG, PDMU versus NG, and PDNMU versus PDMU over-expressed inflammatory markers and miR-24, miR-27, miR-100, miR-126, and miR-133 (p < 0.05). Finally, at the end of follow-up, we observed a significant difference about MACE comparing PDNMU versus NG (n = 27 (36.9%) versus n = 8 (6.4%); p < 0.05), PDNMU versus PDMU (n = 27 (36.9%) versus n = 6 (16.6%); p < 0.05); and PDMU versus NG (n = 6 (16.6%) versus n = 8 (6.4%); p < 0.05). Admission glucose values (HR (hazard ratio) 1.020, CI (confidence of interval) 95% (1.001-1.038), p = 0.029), atheromatous carotid plaque (HR 5.373, CI 95% (1.251-11.079), p = 0.024), and miR-24 (HR 3.842, CI 95% (1.768-19.222), p = 0.011) predicted MACE at 2 years of follow-up. Specific circulating miRs could be over-expressed in pre-diabetics and specifically in PDNMU versus PDMU after endarterectomy. MiR24, hyperglycemia, and atheromatous plaque could predict MACE at 2 years of follow-up.

The secret life of the mitral valve.

In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendineae lengthen: the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor-ß (TGF-ß), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF-ß activation facilitates leaflet growth, excessive TGF-ß activation, as after myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity, and to explain why the equation "large heart = moderate/severe mitral regurgitation" and "small heart = no/mild mitral regurgitation" does not work into the clinical practice.

Ultrasound-guided Erector Spinae Plane Block (US-ESPB)-Anesthetic block: Case report.

The Ultrasound-guided Erector Spinae Plane Block (US-ESPB), used as an anesthesiological block, could represent a safe and effective alternative for thoracic wall surgery especially in fragile, obese patients and those with respiratory and/or hemodynamic problems.

Delirium in ICU patients following cardiac surgery: An observational study.

AIMS AND OBJECTIVES: To observe the clinical and structural factors that can be associated with the post-operative onset of delirium in patients who have undergone heart surgery. BACKGROUND: Several risk factors could contribute to the development of delirium, such as the use of some sedative drugs and a patient's history with certain types of acute chronic disease. However, in the literature, there is little knowledge about the association between delirium in patients who have undergone cardiac surgical intervention and their clinical and environmental predictors. DESIGN: We used an observational design. METHODS: We enrolled 89 hospitalised patients in the ICU. Patients were first evaluated using the Richmond Agitation Sedation Scale and subsequently using the Confusion Assessment Method for the ICU. A linear model of regression was used to identify the predictors of delirium in patients. RESULTS: The patients had an average age of 89 years (SD = 6.9), were predominantly male (84.3%) and were mostly married (79.8%). The majority of patients had been subjected to bypass (80.9%), while 19.1% had undergone the intervention of endoprosthesis. The logistic regression model showed that patient age, the duration of mechanically assisted ventilation, continuous exposure to artificial light and the presence of sleep disorders were predictors of the onset of delirium. CONCLUSION: This study further confirms that clinical aspects such as insomnia and one's circadian rhythm as well as structural elements such as exposure to artificial light are variables that should be monitored in order to prevent and treat the onset of severe post-operative delirium. RELEVANCE TO CLINICAL PRACTICE: Identifying the possible factors that predispose a patient to the onset of delirium during intensive therapy following cardiac surgery, it is fundamental to implement interventions to prevent this syndrome.