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Among the various comorbidities potentially worsening the clinical outcome in patients hospitalized for the acute respiratory syndrome coronavirus-2 (SARS-CoV-2), hypertension is one of the most prevalent. However, the basic mechanisms underlying the development of severe forms of coronavirus disease 2019 (COVID-19) among hypertensive patients remain undefined and the direct association of hypertension with outcome in COVID-19 is still a field of debate. Experimental and clinical data suggest that SARS-CoV-2 infection promotes a rise in blood pressure (BP) during the acute phase of infection. Acute increase in BP and high in-hospital BP variability may be tied with acute organ damage and a worse outcome in patients hospitalized for COVID-19. In this context, the failure of the counter-regulatory renin-angiotensin-system (RAS) axis is a potentially relevant mechanism involved in the raise in BP. It is well recognized that the efficient binding of the Spike (S) protein to angiotensin converting enzyme 2 (ACE2) receptors mediates the virus entry into cells. Internalization of ACE2, downregulation and malfunction predominantly due to viral occupation, dysregulates the protective RAS axis with increased generation and activity of angiotensin (Ang) II and reduced formation of Ang 1,7 . Thus, the imbalance between Ang II and Ang 1-7 can directly contribute to excessively rise BP in the acute phase of SARS-CoV-2 infection. A similar mechanism has been postulated to explain the raise in BP following COVID-19 vaccination ("Spike Effect" similar to that observed during the infection of SARS-CoV-2). S proteins produced upon vaccination have the native-like mimicry of SARS-CoV-2 S protein's receptor binding functionality and prefusion structure and free-floating S proteins released by the destroyed cells previously targeted by vaccines may interact with ACE2 of other cells, thereby promoting ACE2 internalization and degradation, and loss of ACE2 activities., (Copyright © 2022 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)

The role of a dysregulated renin-angiotensin system (RAS) in the pathogenesis of COVID-19 is well recognized. The imbalance between angiotensin II (Ang II) and Angiotensin 1-7 (Ang 1,7 ) caused by the interaction between SARS-CoV-2 and the angiotensin converting enzyme 2 (ACE 2 ) receptors exerts a pivotal role on the clinical picture and outcome of COVID-19. ACE 2 receptors are not the exclusive angiotensinases in nature. Other angiotensinases (PRCP, and POP) have the potential to limit the detrimental effects of the interactions between ACE 2 and the Spike proteins. In the cardiovascular disease continuum, ACE 2 activity tends to decrease, and POP/PRCP activity to increase, from the health status to advanced deterioration of the cardiovascular system. The failure of the counter-regulatory RAS axis during the acute phase of COVID-19 is characterized by a decrease of ACE 2 expression coupled to unchanged activity of other angiotensinases, therefore failing to limit the accumulation of Ang II. COVID-19 vaccines increase the endogenous synthesis of SARS-CoV-2 spike proteins. Once synthetized, the free-floating spike proteins circulate in the blood, interact with ACE 2 receptors and resemble the pathological features of SARS-CoV-2 ("Spike effect" of COVID-19 vaccines). It has been noted that an increased catalytic activity of POP/PRCP is typical in elderly individuals with comorbidities or previous cardiovascular events, but not in younger people. Thus, the adverse reactions to COVID-19 vaccination associated with Ang II accumulation are generally more common in younger and healthy subjects. Understanding the relationships between different mechanisms of Ang II cleavage and accumulation offers the opportunity to close the pathophysiological loop between the risk of progression to severe forms of COVID-19 and the potential adverse events of vaccination., (Copyright © 2022. Published by Elsevier B.V.)

Coronavirus disease 2019 (COVID-19) vaccines proved a strong clinical efficacy against symptomatic or moderate/severe COVID-19 and are considered the most promising approach for curbing the pandemic. However, some questions regarding the safety of COVID-19 vaccines have been recently raised. Among adverse events to vaccines and despite a lack of signal during phase III clinical trials, an increase in blood pressure (BP) after COVID-19 vaccination has been reported as a potential adverse reaction. We systematically analyze this topic and undertook a meta-analysis of available data to estimate the proportion of patients with abnormal BP or raise in BP after vaccination. Six studies entered the final analysis. Overall, studies accrued 357,387 subjects with 13,444 events of abnormal or increased BP. After exclusion of outlier studies, the pooled estimated proportion of abnormal/increased BP after vaccination was 3.20% (95% CI: 1.62-6.21). Proportions of cases of stage III hypertension or hypertensive urgencies and emergencies was 0.6% (95% CI: 0.1% to 5.1%). In conclusion, abnormal BP is not rare after COVID-19 vaccination, but the basic mechanisms of this phenomenon are still unclear and require further research.

Background: Post-operative (POP) atrial fibrillation (AF) is frequent in patients who undergo cardiac surgery. However, its prognostic impact in the long term remains unclear., Methods: We followed 1386 patients who underwent cardiac surgery for an average of 10 ± 3 years. According to clinical history of AF before and after surgery, four subgroups were identified: (1) patients with no history of AF and without episodes of AF during the first 30 days after surgery (control or Group 1, n = 726), (2) patients with no history of AF before surgery in whom new-onset POP AF was detected during the first 30 days after surgery (new-onset POP AF or Group 2, n = 452), (3) patients with a history of paroxysmal/persistent AF before cardiac surgery (Group 3, n = 125, including 87 POP AF patients and 38 who did not develop POP AF), and (4) patients with permanent AF at the time of cardiac surgery (Group 4, n = 83). All-cause mortality was the primary outcome of the study. We tested the associations of potential determinants with all-cause mortality using univariable and multivariable statistical analyses., Results: Overall, 473 patients (34%) died during follow-up. After adjustment for multiple confounders, new-onset POP AF (hazard ratio (HR) = 1.31, 95% confidence interval (CI): 0.90-1.89; p = 0.1609), history of paroxysmal/persistent AF before cardiac surgery (HR = 1.33, 95% CI: 0.71-2.49; p = 0.3736), and permanent AF (Group 4) (HR = 1.55, 95% CI 0.82-2.95; p = 0.1803) were not associated with a significantly increased risk of mortality when compared with Group 1 (patients with no history of AF and without episodes of AF during the first 30 days after surgery). In new-onset POP AF patients, oral anticoagulation was not associated with mortality (HR = 1.13, 95% CI: 0.83-1.54; p = 0.4299)., Conclusions: In this cohort of patients who underwent different types of heart surgery, POP AF was not associated with an increased risk of mortality. In this setting, the role of long-term anticoagulation remains unclear.

Background: Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may cause an acute multiorgan syndrome (coronavirus disease 2019 (COVID-19)), data are emerging on mid- and long-term sequelae of COVID-19 pneumonia. Since no study has hitherto investigated the role of both cardiac and pulmonary ultrasound techniques in detecting such sequelae, this study aimed at evaluating these simple diagnostic tools to appraise the cardiopulmonary involvement after COVID-19 pneumonia., Methods: Twenty-nine patients fully recovered from COVID-19 pneumonia were considered at our centre. On admission, all patients underwent 12-lead electrocardiogram (ECG) and transthoracic echocardiography (TTE) evaluation. Compression ultrasound (CUS) and lung ultrasound (LUS) were also performed. Finally, in each patient, pathological findings detected on LUS were correlated with the pulmonary involvement occurring after COVID-19 pneumonia, as assessed on thoracic computed tomography (CT)., Results: Out of 29 patients (mean age 70 ± 10 years; males 69%), prior cardiovascular and pulmonary comorbidities were recorded in 22 (76%). Twenty-seven patients (93%) were in sinus rhythm and two (7%) in atrial fibrillation. Persistence of ECG abnormalities from the acute phase was common, and nonspecific repolarisation abnormalities (93%) reflected the high prevalence of pericardial involvement on TTE (86%). Likewise, pleural abnormalities were frequently observed (66%). TTE signs of left and right ventricular dysfunction were reported in two patients, and values of systolic pulmonary artery pressure were abnormal in 16 (55%, despite the absence of prior comorbidities in 44% of them). Regarding LUS evaluation, most patients displayed abnormal values of diaphragmatic thickness and excursion (93%), which correlated well with the high prevalence (76%) of pathological findings on CT scan. CUS ruled out deep vein thrombosis in all patients., Conclusions: Data on cardiopulmonary involvement after COVID-19 pneumonia are scarce. In our study, simple diagnostic tools (TTE and LUS) proved clinically useful for the detection of cardiopulmonary complications after COVID-19 pneumonia.

Background and objectives: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Among extra-pulmonary manifestations of COPD, atrial fibrillation (AF) is commonly observed in clinical practice. The coexistence of COPD and AF significantly affects the risk of cardiovascular morbidity and mortality. Nonetheless, the mechanisms explaining the increased risk of vascular events and death associated to the presence of COPD in AF are complex and not completely understood. We analyzed data from an Italian network database to identify markers and mediators of increased vascular risk among subjects with AF and COPD. Materials and Methods: Cross-sectional analysis of the Umbria Atrial Fibrillation (Umbria-FA) Registry, a multicenter, observational, prospective on-going registry of patients with non-valvular AF. Of the 2205 patients actually recruited, 2159 had complete clinical data and were included in the analysis. Results: the proportion of patients with COPD was 15.6%. COPD patients had a larger proportion of permanent AF when compared to the control group (49.1% vs. 34.6%, p < 0.0001) and were more likely to be obese and current smokers. Other cardiovascular risk factors including chronic kidney disease (CKD), peripheral artery disease and subclinical atherosclerosis were more prevalent in COPD patients (all p < 0.0001). COPD was also significantly associated with higher prevalence of previous vascular events and a history of anemia (all p < 0.0001). The thromboembolic and bleeding risk, as reflected by the CHA 2 DS 2 VASc and HAS-BLED scores, were higher in patients with COPD. Patients with COPD were also more likely to have left ventricular (LV) hypertrophy at standard ECG than individuals forming the cohort without COPD ( p = 0.018). Conclusions: AF patients with COPD have a higher risk of vascular complications than AF patients without this lung disease. Our analysis identified markers and mediators of increased risk that can be easily measured in clinical practice, including LV hypertrophy, CKD, anemia, and atherosclerosis of large arteries.

Hypertension is one of the most common chronic diseases in adults and a leading cause of disability and mortality worldwide. Recently, new Guidelines for the diagnosis and management of hypertension have been released in Europe and in the United States, with changes regarding how to diagnose and treat the condition, and the extent to which intensive blood pressure control should be pursued. Important differences between the Guidelines exist in the classification of blood pressure levels and definition of treatment goals. Diagnosis of hypertension starts at 140/90 mmHg for the European Guidelines, and 130/80 mmHg for the US Guidelines. Besides, the European guidelines introduced the concept of "safety boundaries", consisting of BP thresholds not to be exceeded towards lower levels (120 mmHg for age < 65 years, 130 mmHg for older people) because of the fear of important adverse events associated with overtreatment. Such discrepancies can indeed have an impact on treatment attitudes and outcome incidence. Hence, we appraised facts in favor and against each of these controversial issues. In conclusion we believe that, instead of fixing rigid BP targets and boundaries, modern hypertension management should be aimed to achieve in each patient an optimal balance between intensive BP reduction and treatment safety., (Copyright © 2019 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)

Left ventricular (LV) hypertrophy at electrocardiography (ECG) predicts incident atrial fibrillation (AF). However, the diagnostic performance of ECG for diagnosis of LV hypertrophy in patients with AF is still not well characterized. We analyzed 563 hypertensive patients enrolled in the Umbria-Atrial Fibrillation (Umbria-FA) registry, an ongoing prospective observational registry in patients with AF. All patients underwent ECG and standard echocardiography at their entry in the Register. Mean age was 74 years and 43% of patients were women. Prevalence of ECG-LV hypertrophy, defined by Perugia criterion corrected for body mass index, was 23%. Echocardiographic LV mass was the reference standard. Sensitivity, specificity and diagnostic accuracy of ECG-LV hypertrophy were 37.4% (95% confidence interval [CI]: 31.6-43.4), 90.0% (95% CI: 86.0-93.2) and 64.5% (95% CI: 60.4-68.3), respectively. Performance was comparable in patients with AF or sinus rhythm at ECG recording. The area under the receiver-operating characteristic (ROC) curve was 0.622 (95% CI: 0.580-0.664) in the group with AF and 0.662 (95% CI: 0.605-0.720) in that with sinus rhythm (p ​= ​0.266 for comparison). These data suggest that standard ECG is reliable for diagnosis of LV hypertrophy in patients with a history of AF, regardless of the presence of AF or sinus rhythm at the time of ECG recording., (© 2019 The Authors.)

Hypertension is a global public health issue and a major cause of morbidity and mortality. Its prevalence is increasing in many Asian countries, with a number of countries with blood pressure above the global average. Although the average systolic blood pressure is decreasing worldwide since the 1980s at the rate of about 1 mm Hg systolic blood pressure per decade, it is increasing in low-income and middle-income countries, especially in the East and South Asian population. Of note, the much larger base Asian population results in a considerably larger absolute number of individuals affected. When compared with Western countries, hypertension among Asian populations has unique features in terms of its onset, clustering of associated cardiovascular risk factors, complications and outcomes. Moreover, only a minority of hypertensive individuals are receiving treatment and achieving control. Projected number of deaths related to hypertension dramatically increased in the last 25 years in some Asian regions with a disproportionately high mortality and morbidity from stroke compared with Western countries. The relation between blood pressure and the risk of stroke is stronger in Asia than in Western regions. Although new Guidelines for hypertension diagnosis and management have been recently released from Europe and North America, the unique features of Asian hypertensive patients raise concerns on the clinical applicability of Western Guidelines to Asian populations. To this purpose, we critically reviewed key elements from the most updated Guidelines. We also discussed their core concepts to verify the impact on hypertension prevention and management in Asian countries., Competing Interests: Competing interests: None declared.

Introduction: Osteoarthritis constitutes one of the leading causes of pain and disability worldwide with a significant impact on health-care costs. Patients with osteoarthritis are often affected by a number of cardiovascular comorbidities, including hypertension, which is present in about 40% of cases. Just recently, a single tablet combination of amlodipine besylate, a calcium channel blocker, and celecoxib, a nonsteroidal anti-inflammatory drug, indicated for patients for whom treatment with amlodipine for hypertension and celecoxib for osteoarthritis are appropriate, has been recently approved. Areas covered: We reviewed data from clinical studies that investigated safety and efficacy of the combination of amlodipine and celecoxib in hypertensive patients with osteoarthritis published before 31 August 2018. The literature search was conducted using research Methodology Filters. Expert commentary: The advantages of this single formulation over sequential administration include increased compliance, possibly reduced cost, and less likelihood of dosage-related issues. Moreover, this single tablet formulation combines the anti-inflammatory activity of the celecoxib with the systemic vasodilatation induced by the amlodipine. It is a promising treatment for patients with osteoarthritis and hypertension. Nevertheless, celecoxib may cause a variable degree of blood pressure increase and only a small clinical trial has been conducted before approval to assess interactions related to blood pressure effect between these two molecules.

Hypertension is a key risk factor for chronic kidney disease (CKD), but can also be a detrimental consequence of established CKD. Unsurprisingly, the majority of subjects with abnormal creatinine in the general population are also hypertensive, with a huge toll on national health care systems worldwide due to a staggering increase in the risk of cardiovascular complications and end-stage renal disease requiring renal replacement therapy. In this setting, a comprehensive and careful assessment of the whole 24-h blood pressure (BP) profile could be of paramount importance in ensuring a timely diagnosis of hypertension and an optimal therapeutic control. Hence, ambulatory BP monitoring (ABPM) has the potential to become the preferred method for optimal clinical management of CKD patients. ABPM might better define the relationship between BP, target organ damage (TOD), and clinical outcomes. Current evidence suggests that specific day-night BP components, along with average BP values, may have clinical relevance in such patients, despite the suboptimal statistical power of available studies and inconsistencies on the prognostic value of individual BP components. The main aim of our review is to scrutinize the evidence for the usage of ABPM in CKD patients, including the relationship between ambulatory BP recordings and cardiovascular events, and the distinctive features of ABPM in these subjects.

Introduction: Fimasartan is the ninth and latest Angiotensin Receptor Blockers for the treatment of hypertension. Fimasartan is a derivative of losartan in which the imidazole ring has been replaced. It provides a selective type 1 angiotensin II receptor antagonist effect with noncompetitive, in surmountable binding. Fimasartan is rapidly absorbed following oral administration with an oral bioavailability of 18.6 ± 7.2%. Fimasartan is relatively stable in terms of metabolism and more than 90% of circulating fimasartan moieties in the plasma are in the parent form; fecal elimination and biliary excretion are the predominant elimination pathways of fimasartan. Areas covered: We reviewed data from clinical trials that investigated safety and efficacy of fimasartan in hypertension. Expert opinion: Fimasartan proved good efficacy in blood pressure reduction. In large clinical studies,fimasartan showed an excellent safety profile and when combined with hydrochlorothiazide oram lodipine, it showed a better effect on controlling blood pressure than monotherapy. Fimasartan 60-120 mg once daily has also shown an antihypertensive effect over 24-h. Moreover, preclinical studies demonstrated organ-protecting effects of fimasartan. These results make fimasartan an attractive candidate for the treatment of hypertension. However, it remains to test the benefit of using fimasartan on clinical outcomes.

Management of the nasal dorsum remains a challenge in rhinoplasty surgery. Currently, the majority of reduction rhinoplasties results in destruction of the keystone area (K-area), which requires reconstruction with either spreader grafts or spreader flaps, both for aesthetic and functional reasons. This article will present the senior author's current operative technique for dorsal preservation in reduction rhinoplasty based on 320 clinical cases performed over a 5-year period. The author's operative technique is as follows: (1) endonasal approach; (2) removal of a septal strip in the subdorsal area whose shape and height were determined preoperatively; (3) complete lateral, transverse, and radix osteotomies; and (4) dorsal reduction utilizing either a push down operation (PDO) or a let down operation (LDO). The PDO consists of downward impaction of the fully mobilized nasal pyramid and is utilized in patients with smaller humps (Less than 4 mm). The LDO consists of a maxillary wedge resection and is performed in patients who need more than 4 mm of lowering. A total of 320 patients had a dorsal preservation operation (DPO). Postoperatively, there were no dorsal irregularities nor inverted-V deformities. Among our 44 personal revision cases, 27 patients (8.74%) had had a previous DPO, 16 of whom required tip revisions with no further dorsal surgery. Of the remaining 11 patients, the main problems were either hump recurrence and/or lateral deviation of the dorsum or widening of the middle third, which required simple surgical revision. Based on the authors' experience, adoption of a PDO/LDO is justified in selected primary patients. The key question before any primary rhinoplasty procedure should be "Can I keep the nasal dorsum intact?" Precise analysis and surgical execution are required to preserve the dorsal osseocartilaginous vault and K-area. Dorsal preservation results in more natural postoperative dorsum lines and a "not operated" aspect without the need for midvault reconstruction. Moreover, this technique is quick and easy to perform by any rhinoplasty surgeon. Rhinoplasty surgeons should consider incorporating dorsal preservation techniques in their surgical armamentarium rather than relying solely on the Joseph reduction method or an open structure rhinoplasty., (© 2018 The American Society for Aesthetic Plastic Surgery, Inc. Reprints and permission: journals.permissions@oup.com.)

Background/aim: The aim of the present study was to evaluate the safety and the clinical outcome of platelet-rich plasma for the treatment of teno-desmic injures in competition horses., Patients and Methods: From January 2009 to December 2011, 150 sport horses suffering from teno-desmic injuries were treated with no-gelled platelet-concentrate., Results: No horse showed any major adverse reaction as a result of the procedure. Full healing was obtained for 81% of the horses. Twelve percent had clinical improvement and only 7% a failure. Eight percent of cases of relapse were observed. No statistically significant correlation existed between clinical outcome and the area of the lesion. A statistically significant correlation existed between the clinical outcome and the age of the horse., Conclusion: Treatment with platelet-derived growth factors leads to the formation of a tendon with normal morphology and functionality, which translate in the resumption of the agonistic activity for the horses we treated., (Copyright © 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Summary: Sometimes, after local anesthetic injection for surgical procedures of the upper eyelid, it is possible to observe superficial preseptal hematomas or excessive lid swelling that may distort the tissues and obscure surgical landmarks. We present a technique to perform local anesthesia of the upper eyelids, using a 27-gauge needle and a 26-gauge filling cannula, that may decrease the incidence of hematomas and bruising.

Objectives: This study sought to evaluate the possible association of polymorphism of the angiotensin-converting enzyme (ACE) gene with blood pressure and left ventricular mass index (LVMI)., Background: The renin-angiotensin system seems to be involved in the pathogenesis of essential hypertension. Moreover, recent epidemiologic observations demonstrate that many subjects with left ventricular hypertrophy have normal blood pressure levels, suggesting that factors other than hemodynamic overload may contribute to the hypertrophy., Methods: The study included 140 untreated hypertensive outpatients who underwent ambulatory blood pressure monitoring, echocardiographic evaluation and analysis for insertion (I)/ deletion (D) polymorphism in intron 16 of the ACE gene by polymerase chain reaction. Blood pressure was measured at 24 h, and LVMI was calculated by the Devereux formula, in each patient., Results: Left ventricular mass index values (mean +/- SD) were 137 +/- 28 g/m2 in patients with the DD genotype, 125 +/- 27 g/m2 in those with the ID genotype and 115 +/- 27 g/m2 in those with II genotype. The frequencies of the DD, ID and II genotypes were 45.71% (n = 64), 46.42% (n = 65) and 7.85% (n = 11), respectively, and were in Hardy-Weinberg equilibrium. The strongest association between left ventricular mass and DD genotype in our cohort appeared to be an independent cardiovascular risk factor (DD vs. ID: odds ratio [OR] 2.497, 95% confidence interval [CI] interval 1.158 to 5.412, p < 0.05; DD vs. II: OR 6.577, 95% CI 1.169 to 28.580, p < 0.02)., Conclusions: Our data show that the LVMI was significantly enhanced in patients with the DD genotype.