Varicella zoster virus and cardiovascular diseases.

Varicella zoster virus (VZV) is a Herpesviridae family double-stranded DNA virus that only affects humans. The first clinical manifestation appears to be varicella, typical of childhood. VZV, on the other hand, becomes latent in ganglion neurons throughout the neuroaxis after primary infection. The VZV reactivates and travels along peripheral nerve fibers in the elderly and immunocompromised individuals, resulting in Zoster. It can, however, spread centrally and infect cerebral and extracranial arteries, resulting in vasculopathy, which can lead to transient ischemic attacks, strokes, aneurysms, cavernous sinus thrombosis, giant cell arteritis, and granulomatous aortitis. Although the mechanisms of virus-induced pathological vascular remodeling are not fully understood, recent research indicates that inflammation and dysregulation of ligand-1 programmed death play a significant role. Few studies, on the other hand, have looked into the role of VZV in cardiovascular disease. As a result, the purpose of this review is to examine the relationship between VZV and cardiovascular disease, the efficacy of the vaccine as a protective mechanism, and the target population of heart disease patients who could benefit from vaccination.

Study of endothelial function and vascular stiffness in patients affected by dilated cardiomyopathy on treatment with sacubitril/valsartan.

BACKGROUND: The multiple beneficial effects of sacubitril/valsartan in the treatment of heart failure with reduced ejection fraction are vastly known, but still no or few mentions have been made regarding its effects on endothelial dysfunction and arterial stiffness. PATIENTS AND METHODS: To understand more deeply if sacubitril/valsartan may have a role on endothelial function and arterial stiffness, 15 patients with dilated cardiomyopathy with reduced left ventricular ejection fraction (LVEF) were evaluated through transthoracic echocardiography, peripheral arterial tonometry (EndoPAT®) and applanation tonometry (SphygmoCor® Px system). These noninvasive exams were performed at the beginning of the study and after 6 months of sacubitril/valsartan treatment. RESULTS: Aortic stiffness parameters didn't differ after 6 months of treatment. Augmentation pressure (P=0.889), augmentation index (P=0.906) and sphygmic wave velocity (P=0.263) increased slightly, but they weren't found to be statistically significant. Systolic, diastolic, and differential central arterial pressure didn't differ at the beginning and at the end of the study. RHI (reactive hyperemia index) increased significantly after 6 months (P=0.001) as well as augmentation index corrected for 75 bpm. Ejection fraction (32.21% ± 5.7 to 38.43% ± 8.4; P=0.010) and diastolic dysfunction degree (P=0.021) improved. There was an improvement in mitral regurgitation that wasn't statistically significant (P=0.116). TAPSE didn't change while pulmonary systolic arterial pressure increased, although not significantly (22.83 mmHg ± 4 to 27.33 mmHg ± 6; P=0.068) and within the normal range values. CONCLUSIONS: Even though in a study with a limited number of patients, sacubitril/valsartan improved endothelial function, left ventricular function, MR, and diastolic function significantly in patients with dilated cardiomyopathy and reduced LVEF. It showed no effects on vascular stiffness.

Cardiac biomarkers and mortality in COVID-19 infection: A review.

Lots of meta-analysis emphasize that a great number of hospitalized patients with moderate and severe forms of COVID-19 developed acute myocardial damage, defined as an increase of cardiac biomarkers, such N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), creatine kinase-myocardial band (CK-MB) and of all type of troponins. The highest mortality rate is related with progressively increasing biomarkers levels and with a history of cardiovascular disease. In fact, the biomarkers dosage should be considered as a prognostic marker in all patients with COVID-19 disease at admission, during hospitalization and in the case of clinical deterioration. The purpose of this review is to evaluate cardiovascular prognostic factors in COVID-19 disease throughout the analysis of cardiac biomarkers to early identify the most serious patients and to optimize their outcomes.

Endothelial dysfunction in COVID-19 patients assessed with Endo-PAT2000.

It has been widely reported that the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) attaches human cells by using the Angiotensin Converting Enzyme 2 (ACE2) receptor, but vascular impairment described during coronavirus disease 2019 (COVID-19) infection is primarily due to the direct involvement of the endothelial cells by the virus or secondarily to the inflammatory host response is currently unknown. We therefore aimed to demonstrate in vivo the presence of endothelial dysfunction in six COVID-19 patients without cardiovascular risk factors or pre-existing cardiac condition, using the Endo-PAT 2000, a device able to measure endothelial vasodilation function in a rapid and non-invasive way. Four patients were positive for endothelial dysfunction, with RHI values between 1.13-1.56 (average value 1.32, normal values >1.67); in one of the two negative patients the reported RHI value was slightly above the cutoff (1.72). Our findings confirm that COVID-19 patients are at higher risk of developing endothelial dysfunction. In addition, our results demonstrate that endothelial impairment may occur even in the absence of cardiovascular risk factors.

Thrombotic risk in patients with COVID-19.

Emerging evidences prove that the ongoing pandemic of coronavirus disease 2019 (COVID-19) is strictly linked to coagulopathy even if pneumonia appears as the major clinical manifestation. The exact incidence of thromboembolic events is largely unknown, so that a relative significant number of studies have been performed in order to explore thrombotic risk in COVID-19 patients. Cytokine storm, mediated by pro-inflammatory interleukins, tumor necrosis factor α and elevated acute phase reactants, is primarily responsible for COVID-19-associated hypercoagulopathy. Also comorbidities, promoting endothelial dysfunction, contribute to a higher thromboembolic risk. In this review we aim to investigate epidemiology and clarify the pathophysiological pathways underlying hypercoagulability in COVID-19 patients, providing indications on the prevention of thromboembolic events in COVID-19. Furthermore we aim to reassume the pathophysiological paths involved in COVID-19 infection.

Durability at 19 Years of Quadrangular Resection With Annular Plication for Mitral Regurgitation.

BACKGROUND: We report the long-term (19 years) clinical and echocardiographic results of the quadrangular resection with annular plication and annuloplasty. METHODS: Included were 145 consecutive patients (mean age, 58 ± 11.1 years; left ventricular ejection fraction, 0.59 ± 0.095) with severe degenerative mitral regurgitation due to posterior leaflet prolapse/flail who underwent quadrangular resection of the posterior leaflet combined with ring (127 patients [87.5%]) or pericardium (18 patients [12.5%]) annuloplasty. RESULTS: No hospital deaths occurred. At hospital discharge, all patients but 1 had none or trivial mitral regurgitation. Follow-up was 97% complete (median, 19 years; interquartile range, 18 to 20 years). At 20 years, the overall survival was 74% ± 3.7%. At 19 years, cumulative incidence function of cardiac death with noncardiac death as a competing risk was 9.9% ± 2.5% (95% confidence interval [CI], 5.7% to 15.5%). Age was the only significant predictor of cardiac death (hazard ratio, 1.1; 95% CI, 1.0 to 1.1; p = 0.01) at multivariate analysis. Only 6 patients (4%) were reoperated on for recurrent severe mitral regurgitation. At 19 years, cumulative incidence function of reoperation and recurrence of mitral regurgitation 3+ or higher with death as a competing risk was 4.3% ± 1.7% (95% CI, 1.7% to 8.8%) and 8.8% ± 2.8% (95% CI, 4.3% to 15.5%), respectively. Indeed, only 11 patients (8%) had recurrent mitral insufficiency 3+ or higher. No predictor of reoperation and recurrence of mitral regurgitation 3+ or higher was identified. At the last follow-up, moderate mitral regurgitation (2+/4+) was detected in 14 patients (10%). CONCLUSIONS: Quadrangular resection with annular plication for posterior leaflet prolapse, combined with annuloplasty, is associated with a very low probability of reoperation and recurrent mitral regurgitation for up to 2 decades after the operation. These results provide reference values to which all of the other more recently introduced surgical and transcatheter options need to be compared.