Nutritional Status and Recurrent Major Cardiovascular Events Following Acute Myocardial Infarction-A Follow-Up Study in a Primary Percutaneous Coronary Intervention Center.

BACKGROUND: Acute myocardial infarction is often accompanied by malnutrition, which is associated with an imbalance between catabolic and anabolic processes. This ultimately leads to cardiac cachexia, which worsens the patient's prognosis. We aimed to assess the correlation between nutritional status, assessed using the controlling nutritional status (CONUT) score, and the rate of major cardiovascular adverse events (MACE). METHODS: The present investigation was a non-randomized, prospective, observational study in which 108 patients with acute myocardial infarction were included. Nutritional status was assessed using the CONUT score. Based on the CONUT score, the patients were divided as follows: Group 1-normal or mild nutritional status (CONUT < 3 points, n = 76), and Group 2-moderate to severe nutritional deficiency (CONUT ≥ 3 points, n = 32). Demographic, echocardiographic, and laboratory parameters were obtained for all patients, as well as the MACE rate at 1 and 3 months of follow-up. RESULTS: The MACE occurred more frequently in patients with impaired nutritional status at both 1-month follow-up (46.9% versus 9.2%; p < 0.0001) and 3-month follow-up (68.8% versus 10.5%; p < 0.0001). In terms of cardiovascular events, patients with poor nutritional status, with a CONUT score ≥ 3, presented more frequent non-fatal myocardial infarction, stroke, revascularization procedure, and ventricular arrhythmia. Also, the number of cardiovascular deaths was higher in the undernourished group. CONCLUSIONS: This study found that patients with poor nutritional status experienced inflammatory status, frailty, and cardiovascular events more often than those with normal nutritional status at 1-month and 3-month follow-up after an acute myocardial infarction.

CT-Assessment of Epicardial Fat Identifies Increased Inflammation at the Level of the Left Coronary Circulation in Patients with Atrial Fibrillation.

Background: Atrial fibrillation (AF) can often be triggered by an inflammatory substrate. Perivascular inflammation may be assessed nowadays using coronary computed tomography angiography (CCTA) imaging. The new pericoronary fat attenuation index (FAI HU) and the FAI Score have prognostic value for predicting future cardiovascular events. Our purpose was to investigate the correlation between pericoronary fat inflammation and the presence of AF among patients with coronary artery disease. Patients and methods: Eighty-one patients (mean age 64.75 ± 7.84 years) who underwent 128-slice CCTA were included in this study and divided into two groups: group 1 comprised thirty-six patients with documented AF and group 2 comprised forty-five patients without a known history of AF. Results: There were no significant differences in the absolute value of fat attenuation between the study groups (p > 0.05). However, the mean FAI Score was significantly higher in patients with AF (15.53 ± 10.29 vs. 11.09 ± 6.70, p < 0.05). Regional analysis of coronary inflammation indicated a higher level of this process, especially at the level of the left anterior descending artery (13.17 ± 7.91 in group 1 vs. 8.80 ± 4.75 in group 2, p = 0.008). Conclusions: Patients with AF present a higher level of perivascular inflammation, especially in the region of the left coronary circulation, and this seems to be associated with a higher risk of AF development.

Oxidative Stress, Inflammation, and Mitochondrial Dysfunction: A Link between Obesity and Atrial Fibrillation.

The adipose tissue has long been thought to represent a passive source of triglycerides and fatty acids. However, extensive data have demonstrated that the adipose tissue is also a major endocrine organ that directly or indirectly affects the physiological functions of almost all cell types. Obesity is recognized as a risk factor for multiple systemic conditions, including metabolic syndrome, type 2 diabetes mellitus, sleep apnea, cardiovascular disorders, and many others. Obesity-related changes in the adipose tissue induce functional and structural changes in cardiac myocytes, promoting a wide range of cardiovascular disorders, including atrial fibrillation (AF). Due to the wealth of epidemiologic data linking AF to obesity, the mechanisms underlying AF occurrence in obese patients are an area of rich ongoing investigation. However, progress has been somewhat slowed by the complex phenotypes of both obesity and AF. The triad inflammation, oxidative stress, and mitochondrial dysfunction are critical for AF pathogenesis in the setting of obesity via multiple structural and functional proarrhythmic changes at the level of the atria. The aim of this paper is to provide a comprehensive view of the close relationship between obesity-induced oxidative stress, inflammation, and mitochondrial dysfunction and the pathogenesis of AF. The clinical implications of these mechanistic insights are also discussed.

The Association between Apolipoprotein B, Cardiovascular Risk Factors and Subclinical Atherosclerosis-Findings from the SEPHAR National Registry on Hypertension in Romania.

The present study aimed to investigate the association between apolipoprotein B (Apo B) and classical features associated with clinical or subclinical atherosclerosis. A total of 811 adult patients from the general Romanian population, included in the national SEPHAR registry on hypertension, were divided into two groups based on Apo B value (low versus high Apo B with a cut-off established at 130 mg/dL) and subsequently into four subgroups according to the cut-offs recommended by the 2021 ESC Guidelines on Cardiovascular Disease Prevention. In all patients, lipid profile, uric acid, full blood count and presence of significant carotid plaques were assessed. Apo B levels were positively correlated with proatherogenic lipids (total cholesterol, triglycerides and LDL-cholesterol, p < 0.0001) and negatively correlated with HDL cholesterol (all p < 0.05). In comparison with patients with low Apo B levels, those with elevated Apo B levels more frequently presented significant carotid plaques (17% vs. 19% vs. 28% vs. 46%, p < 0.0001). Univariate regression analysis identified a strong association between the level of uric acid and increased value of Apo B in the four subgroups (uric acid 4.8 +/- 1.3 vs. 5 +/- 1.6 vs. 5.1 +/- 1.5 vs. 5.8 +/- 1.6, r = 0.2, p < 0.0001). The results of this nationwide registry on hypertension in Romania indicate that high Apo B may be considered as a risk factor for CVD, promoting atherosclerosis and associated with increased expression of classical markers of clinical or subclinical CVD.

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats.

Animal studies have brought important insights into our understanding regarding atrial fibrillation (AF) pathophysiology and therapeutic management. Reentry, one of the main mechanisms involved in AF pathogenesis, requires a certain mass of myocardial tissue in order to occur. Due to the small size of the atria, rodents have long been considered 'resistant' to AF. Although spontaneous AF has been shown to occur in rats, long-term follow-up (up to 50 weeks) is required for the arrhythmia to occur in those models. The present work describes an experimental protocol of transesophageal atrial burst pacing for rapid and efficient induction of AF in rats. The protocol can be successfully used in rats with healthy or remodeled hearts, in the presence of a wide variety of risk factors, allowing the study of AF pathophysiology, identification of novel therapeutic targets, and evaluation of novel prophylactic and/or therapeutic strategies.

Is There a Link between COVID-19 Infection, Periodontal Disease and Acute Myocardial Infarction?

Both periodontal disease and atherosclerosis are chronic disorders with an inflammatory substrate that leads to alteration of the host's immune response. In PD, inflammation is responsible for bone tissue destruction, while in atherosclerosis, it leads to atheromatous plaque formation. These modifications result from the action of pro-inflammatory cytokines that are secreted both locally at gingival or coronary sites, and systemically. Recently, it was observed that in patients with PD or with cardiovascular disease, COVID-19 infection is prone to be more severe. While the association between PD, inflammation and cardiovascular disease is well-known, the impact of COVID-19-related inflammation on the systemic complications of these conditions has not been established yet. The purpose of this review is to bring light upon the latest advances in understanding the link between periodontal-cardiovascular diseases and COVID-19 infection.

Periodontal Disease Is Associated with Increased Vulnerability of Coronary Atheromatous Plaques in Patients Undergoing Coronary Computed Tomography Angiography-Results from the Atherodent Study.

The present study aimed to investigate the link between the severity of periodontal disease (PD), coronary calcifications and unstable plaque features in patients who underwent coronary computed tomography for unstable angina (UA). Fifty-two patients with UA, included in the ATHERODENT trial (NCT03395041), underwent computed tomographic coronary angiography (CCTA) and dental examination. Based on the median value of the periodontal index (PI), patients were assigned to the low periodontal index (LPI) group (PI < 22) and a high periodontal index (HPI) group (PI > 22). Patients with HPI had higher plaque volume (p = 0.013) and noncalcified plaque volume (p = 0.0003) at CCTA. In addition, the presence of vulnerability features in the atheromatous plaques was significantly correlated with PI (p = 0.001). Among periodontal indices, loss of gingival attachment (p = 0.009) and papillary bleeding index (p = 0.002) were strongly associated with high-risk plaques. PI significantly correlated with coronary calcium score (r = 0.45, p = 0.0008), but not with traditional markers of subclinical atherosclerosis. Overall, this subgroup analysis of the ATHERODENT study indicates that patients with advanced PD and UA present a higher amount of calcium in the coronary tree and have a more vulnerable phenotype of their culprit plaques.