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Objectives Cardiac magnetic resonance imaging (CMRI) is increasingly used to evaluate cardiac involvement in SSc. We assessed changes, including inflammatory and/or fibrotic myocardial lesions detected by CMRI, following therapeutic interventions for SSc-associated symptomatic myocarditis. Methods In this retrospective study, myocarditis was diagnosed by CMRI (2018 revised Lake Louise criteria) in 14 diffuse and 4 limited SSc patients [16/18 women, age 56 years (s.d. 11), disease duration 8 years (s.d. 11), 17/18 with lung involvement] with cardiac symptoms and abnormal findings on echocardiography (4/18) and/or in 24-hour Holter monitoring (12/14). CMRI was repeated after 8 months (s.d. 3) following administration of cyclophosphamide (n = 11, combined with corticosteroids in 3 and rituximab in 1), mycophenolate (n = 1), tocilizumab (n = 1), methotrexate/corticosteroids (n = 2), corticosteroids (n = 1) or autologous stem cell transplantation (n = 2). Results Functional cardiac improvement was evident by increases in left [by 5.8% (s.d. 7.8), P = 0.006] and right ventricular ejection fraction [by 4.5% (s.d. 11.4), P = 0.085] in the second CMRI compared with the first. Notably, late gadolinium enhancement, currently considered to denote replacement fibrosis, decreased by 3.1% (s.d. 3.8; P = 0.003), resolving in six patients. Markers of myocardial oedema, namely T2 ratio and T2 mapping, decreased by 0.27 (s.d. 0.40; P = 0.013) and 6.0 (s.d. 7; P = 0.025), respectively. Conversely, both T1 mapping, considered to reflect acute oedema and diffuse fibrosis, and extracellular volume fraction, reflecting diffuse fibrosis, remained unchanged. Conclusions CMRI may distinguish between reversible inflammatory/fibrotic and irreversible fibrotic lesions in SSc patients with active myocarditis, confirming the unique nature of primary cardiac involvement in SSc. Whether, and how, CMRI should be used to monitor treatment effects in SSc-associated myocarditis warrants further study.

Chronic kidney disease (CKD) is associated with a higher incidence of cardiovascular death especially as the disease progresses and patients are on long-term dialysis treatment. Left ventricular (LV) dysfunction and cardiac deformation measured by speckle tracking echocardiography seem to play an important prognostic role in several different specific populations.Τhe prognostic value of strain analysis measurements, including the novel diastolic parameters such as left atrial (LA) strain, in patients with end-stage renal disease on dialysis (stage 5 CKD).67 patients (mean age 62.3 ± 11.8, 65.7% men) with stage 5 CKD (45 on hemodialysis and 22 on peritoneal dialysis) were enrolled in the study protocol. The mean duration of dialysis was 102.48 ± 84.98 months. Mean follow-up lasted seven years.Most of the study population had normal or mildly impaired systolic function with a mean LV ejection fraction of 49.17% (± 10.41) while 70% of patients had impaired LV global longitudinal strain, mean 14.35% (± 4.49). Regarding LA strain parameters the mean LA reservoir, LA conduit, and LA contractile reserve were 24.11% (± 12.61), 10.56% (± 5.88), and 13.60% (± 9.15) respectively. Thus 50% of the population had impaired LA strain. Logistic regression analysis showed that of the various echocardiographic parameters LV ejection fraction, LV global longitudinal strain, and the conduit phase of LA strain were significantly associated with total prognosis (p = 0.009, p = 0.007, p = 0.05). The conduit element of LA strain was the strongest predictor among them, when adjusted for age (OR = 0.77 p = 0.04).Left ventricular diastolic dysfunction is an important prognostic factor in patients with advanced CKD on long-term dialysis, without known CAD. The novel echocardiographic parameters such as LA strain could add valuable information to the overall cardiac evaluation of this specific population.

Systematic evidence on the prevalence and clinical outcome of transthyretin amyloidosis (ATTR) is missing. We explored: (i) the prevalence of cardiac amyloidosis in various patient subgroups, (ii) survival estimates for ATTR subtypes, and (iii) the effects of novel therapeutics on the natural course of disease.A systematic review of literature published in MEDLINE before 31 December 2021 was performed for the prevalence of cardiac amyloidosis and all-cause mortality of ATTR patients. Extracted data included sample size, age, sex, and all-cause mortality at 1, 2, and 5 years. Subgroup analyses were performed for ATTR subtype, that is, wild-type ATTR (wtATTR) versus hereditary ATTR (hATTR), hATTR genotypes, and treatment subgroups. We identified a total of 62 studies (n = 277 882 individuals) reporting the prevalence of cardiac amyloidosis, which was high among patients with a hypertrophic cardiomyopathy phenotype, heart failure with preserved ejection fraction, and the elderly with aortic stenosis. Data on ATTR mortality were extracted from 95 studies (n = 18 238 ATTR patients). Patients with wtATTR were older (p = 7 × 10sup-10/sup) and more frequently male (p = 5 × 10sup-20/sup) versus hATTR. The 2-year survival of ATTR was 73.3% (95% confidence interval [CI] 70.9-75.7); for non-subtyped ATTR 70.4% (95% CI 66.9-73.9), for wtATTR 76.0% (95% CI 73.0-78.9]) and for hATTR 77.2% (95% CI 74.0-80.4); in meta-regression analysis, wtATTR was associated with higher survival after adjusting for confounders. There was an interaction between survival and hATTR genotypes (p = 10sup-15/sup, Val30Met having the lowest and Val122Ile/Thr60Ala the highest mortality). ATTR 2-year survival was higher on tafamidis/patisiran compared to natural disease course (79.9%, 95% CI 74.4-85.3 vs. 72.4%, 95% CI 69.8-74.9, p lt; 0.05).We report the prevalence of ATTR in various population subgroups and provide survival estimates for the natural course of disease and the effects of novel therapeutics. Important gaps in worldwide epidemiology research in ATTR were identified.

Cardiac magnetic resonance (CMR) imaging has been established as a valuable diagnostic tool in the assessment of pericardial diseases by providing information on cardiac anatomy and function, surrounding extra-cardiac structures, pericardial thickening and effusion, characterization of pericardial effusion, and the presence of active pericardial inflammation from the same scan. In addition, CMR imaging has excellent diagnostic accuracy for the non-invasive detection of constrictive physiology evading the need for invasive catheterization in most instances. Growing evidence in the field suggests that pericardial enhancement on CMR is not only diagnostic of pericarditis but also has prognostic value for pericarditis recurrence, although such evidence is derived from small patient cohorts. CMR findings could also be used to guide treatment de-escalation or up-titration in recurrent pericarditis and selecting patients most likely to benefit from novel treatments such as anakinra and rilonacept. This article is an overview of the CMR applications in pericardial syndromes as a primer for reporting physicians. We sought to provide a summary of the clinical protocols used and an interpretation of the major CMR findings in the setting of pericardial diseases. We also discuss points that are less well clear and delineate the strengths and weak points of CMR in pericardial diseases.

Background This is a case report of a patient with Anderson–Fabry disease (AFD) due to the D313Y variant on the a-galactosidase A (GLA) gene on migalastat treatment and severe chronic kidney disease referred to our unit to assess possible cardiac involvement. Case summary A 53-year-old man with chronic kidney disease due to AFD and a medical history of revascularized coronary artery disease, chronic atrial fibrillation, and arterial hypertension was referred to our unit for evaluation of possible cardiac involvement in the context of AFD. Biochemical evaluation reported reduced serum alpha-galactosidase A activity and borderline abnormal serum lyso-Gb3 enzyme activity. The patient had also history of acroparesthesias, dermatological presentation of multiple angiokeratomas, severe kidney impairment with an estimated glomerular filtration rate (eGFR) of 30 mL/min/1.73m² by the age of 16, and microalbuminuria that cumulatively set the diagnosis of AFD. Transthoracic echocardiogram showed left ventricular concentric hypertrophy with left ventricular ejection fraction of 45%. Cardiac magnetic resonance showed findings in keeping with ischaemic heart disease (IHD), i.e. akinesia and subendocardial scarring of the basal anterior and the entirety of the septum and the true apex; in addition, there was severe asymmetrical hypertrophy of the basal anteroseptum (max 18 mm), evidence of low-grade myocardial inflammation, and mid-wall fibrosis of the basal inferior and inferolateral wall, suggesting a cardiomyopathic process–myocardial disease which could not be explained solely by IHD or well-controlled hypertension. Discussion This is the first case of possible cardiac involvement in a patient with AFD due to the D313Y variant. This case demonstrates the diagnostic challenges of cardiac involvement in AFD, especially in the presence of a concomitant underlying pathology.

Since 2015, when ESC guidelines for the diagnosis and management of pericardial diseases were published, ongoing research has enhanced the current state of knowledge on acute pericarditis. This review is an update on the latest developments in this field.In recurrent acute pericarditis, autoinflammation has been included among causative mechanisms restricting the vague diagnoses of "idiopathic" pericarditis. Cardiac magnetic resonance that detects ongoing pericardial inflammation may guide treatment in difficult-to-treat patients. Development of risk scores may assist identification of patients at high risk for complicated pericarditis, who should be closely monitored and aggressively treated. Treatment with IL-1 inhibitors has been proven efficacious in recurrent forms with a good safety profile. Finally, acute pericarditis has recently attracted great interest as it has been reported among side effects post COVID-19 vaccination and may also complicate SARS-CoV-2 infection. Recent advancements in acute pericarditis have contributed to a better understanding of the disease allowing a tailored to the individual patient approach. However, there are still unsolved questions that require further research.

Pericardial effusion (PEF) is a common and challenging pericardial syndrome with a variety of clinical manifestations ranging from asymptomatic, incidentally uncovered small PEFs, to life-threatening cardiac tamponade.This review focuses on the pathophysiology, epidemiology, aetiology, classification, clinical findings, diagnostic work-up, management, and outcome of PEFs. Particular emphasis has been given on the most recent evidence concerning the contribution of imaging for the detection, differential diagnosis, and evaluation of the haemodynamic impact of PEFs on the diastolic filling of the heart. Moreover, simplified algorithms for PEF triage and management have been included.The management of patients with PEFs is mainly based on four parameters, namely, haemodynamic impact on diastolic function, elevation of inflammatory markers, presence of a specific underlying condition known to be associated with PEF, and finally size and duration of the effusion. Novel data have contributed to change our view towards large, asymptomatic, 'idiopathic' PEFs and dictated a rather conservative approach in most cases. It is also stressed that there is a compelling need for additional research, which is essential for tailored treatments aiming at the improvement of quality of life and containment of health care costs.

Annual arrhythmic sudden cardiac death ranges from 0.6% to 4% in ischemic cardiomyopathy (ICM), 1% to 2% in non-ischemic cardiomyopathy (NICM), and 1% in hypertrophic cardiomyopathy (HCM). Towards a more effective arrhythmic risk stratification (ARS) we hereby present a two-step ARS with the usage of seven non-invasive risk factors: Late potentials presence (≥ 2/3 positive criteria), premature ventricular contractions (≥ 30/h), non-sustained ventricular tachycardia (≥ 1episode/24 h), abnormal heart rate turbulence (onset ≥ 0% and slope ≤ 2.5 ms) and reduced deceleration capacity (≤ 4.5 ms), abnormal T wave alternans (≥ 65μV), decreased heart rate variability (SDNN70ms), and prolonged QT

To fight the COVID-19 pandemic, messenger RNA (mRNA) vaccines were the first to be adopted by vaccination programs worldwide. We sought to investigate the short-term effect of mRNA vaccine administration on endothelial function and arterial stiffness. Thirty-two participants (mean age 37 ± 8 years, 20 men) who received the BNT162b2 mRNA COVID-19 vaccine were studied in three sessions in a sequence-randomized, sham-controlled, assessor-blinded, crossover design. The primary outcome was endothelial function (assessed by brachial artery flow-mediated dilatation (FMD)), and the secondary outcomes were aortic stiffness (evaluated with carotid-femoral pulse wave velocity (PWV)) and inflammation (measured by high-sensitivity C-reactive protein (hsCRP) in blood samples). The outcomes were assessed prior to and at 8 h and 24 h after the 1st dose of vaccine and at 8 h, 24 h, and 48 h after the 2nd dose. There was an increase in hsCRP that was apparent at 24 h after both the 1st dose (-0.60 [95% confidence intervals [CI]: -1.60 to -0.20], p = 0.013) and the 2nd dose (maximum median difference at 48 h -6.60 [95% CI: -9.80 to -3.40], p 0.001) compared to placebo. The vaccine did not change PWV. FMD remained unchanged during the 1st dose but decreased significantly by 1.5% (95% CI: 0.1% to 2.9%, p = 0.037) at 24 h after the 2nd dose. FMD values returned to baseline at 48 h. Our study shows that the mRNA vaccine causes a prominent increase in inflammatory markers, especially after the 2nd dose, and a transient deterioration of endothelial function at 24 h that returns to baseline at 48 h. These results confirm the short-term cardiovascular safety of the vaccine.

Syncope, whose cause is unknown after an initial assessment, has an uncertain prognosis. It is critical to identify patients at the highest risk who may require a pacemaker and to identify the cause of recurrent syncope to prescribe proper therapy. The aim of this study was to evaluate the effect of permanent pacing on the incidence of syncope in patients with unexplained syncope and electrophysiology study (EPS)-proven atrioventricular (AV) node disease.This was an observational study based on a prospective registry of 236 consecutive patients (60.20 ± 18.66 years, 63.1% male, 60.04 ± 9.50 bpm) presenting with recurrent unexplained syncope attacks admitted to our hospital for invasive EPS. The decision to implant a permanent pacemaker was made in all cases by the attending physicians according to the results of the EPS. A total of 135 patients received the antibradycardia pacemaker (ABP), while 101 patients were declined.The mean of reported syncope episodes was 1.97 ± 1.10 (or presyncope 2.17 ± 1.50) before they were referred for a combined EP-guided diagnostic and therapeutic approach. Over a mean follow-up of approximately 4 years (49.19 ± 29.58 months), the primary outcome event (syncope) occurred in 31 of 236 patients (13.1%), and 6 of 135 (4.4%) patients in the ABP group as compared to 25 of 101 (24.8%) in the no pacemaker group (p 0.001).Among patients with a history of unexplained syncope, a set of positivity criteria for the presence of EPS-defined AV node disease identifies a subset of patients who will benefit from permanent pacing.

Background Measurement of biomarkers of vascular inflammation is advocated for the risk stratification for coronary heart disease (CHD). Objectives To systematically explore the added valu...

Venous thromboembolism (VTE), clinically presented as deep-vein thrombosis (DVT) or pulmonary embolism (PE), constitutes a major global healthcare concern with severe complications, long-term morbidity, and mortality. Although several clinical, genetic, and acquired risk factors for VTE have been identified, the molecular pathophysiology and mechanisms of disease progression remain poorly understood. Anticoagulation has been the cornerstone of therapy for decades, but data is sparse regarding primary and secondary VTE prevention, as well as optimal therapy duration. In this review, we discuss the role of factor Xa in the coagulation cascade and the different choices of anticoagulation therapy based on patients’ predisposing risk factors and risk of event recurrence. Further, we compare newer agents to traditional anticoagulation treatment based on the most recent studies and guidelines.

We aimed to identify the optimal cutoff SAGE score for Brazilian hypertensive patients who had their pulse wave velocity (PWV) measured with oscillometric devices. A retrospective analysis of patients who underwent central blood pressure measurement using a validated oscillometric device, the Mobil-O-Graph® (IEM, Stolberg, Germany), between 2012 and 2019 was performed. Patients with arterial hypertension and available data on all SAGE parameters were selected. An ROC curve was constructed using the Youden index to define the best score to identify patients at high risk for high PWV. A total of 837 patients met the criteria for SAGE and diagnosis of hypertension. The median age was 59.0 years (interquartile range [IQR]: 47.0-68.0), and 50.7% of the patients were women. The following comorbidities and conditions were present: dyslipidemia (37.4%), diabetes (20.7%), a body mass index score ≥30 kg/m2 (36.6%), use of antihypertensive drugs (69.5%), and smoking (18.3%). The median peripheral blood pressure was 128 mmHg (IQR: 117-138 mmHg) for systolic and 81 mmHg (IQR: 73-90 mmHg) for diastolic blood pressure. The median PWV was 8.3 m/s (7.1-9.8 m/s), and the prevalence of high PWV (≥10 m/s) was 22.9% (192 patients). A cutoff SAGE score ≥8 was effective at identifying a high risk of PWV ≥ 10 m/s, achieving 67.19% sensitivity (95% CI: 60.1-73.8) and 93.95% specificity (95% CI: 91.8-95.7). With this cutoff point, 1 out of every 5 treated hypertensive patients would be referred for a PWV measurement. A SAGE score of ≥8 identified Brazilian hypertensive patients with a high risk of future cardiovascular events (PWV ≥ 10 m/s).

Despite the availability of lipid-lowering therapies (LLTs) that are safe and effective, the overall rate of low-density lipoprotein cholesterol (LDL-C) control at a population level in real-life studies is low. Higher-intensity treatment, earlier intervention, and longer-term treatment have all been shown to improve outcomes. However, in clinical practice, actual exposure to LLT is a product of the duration and intensity of, and adherence to, the treatment. To increase exposure to LLTs, the European Society of Cardiology guidelines recommended a stepwise optimization of LLTs by increasing statin intensity to the maximally tolerated dose, with subsequent addition of ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. Evidence from randomized controlled trials performed in a range of patients suggested that adding ezetimibe to statins rather than doubling the statin dose resulted in significantly more patients at LDL-C goal and significantly fewer patients discontinuing treatment because of adverse events. In addition, data showed that combination treatments effectively increased exposure to LLT. Despite these data and recommendations, optimization of LLT is often limited to increasing statin dose. Therapeutic inertia and poor treatment adherence are significant and prevalent barriers to increasing treatment exposure. They are known to be influenced by pill burden and complexity of treatment. Single-pill combinations provide a strategic approach that supports the intensification of treatment without increasing pill burden or treatment complexity. Single-pill combinations, compared with free associations, have been shown to increase the adherence to LLT and the percentage of patients at LDL-C goal.

Degenerative aortic valve stenosis is the most common primary valve disease and a significant cause of cardiovascular morbidity and mortality. In an era when new techniques for the management of aortic stenosis are gaining ground, the understanding of this disease is more important than ever to optimize treatment. So far, the focus has been placed on the assessment of the valve itself. However, the role that the arterial system plays in the pathogenesis and natural history of the disease needs to be further elucidated. Arteriosclerosis, when it coexists with a stenotic valve, augments the load posed on the left ventricle contributing to greater impairment of cardiovascular function. Arterial stiffness, a well-established predictor for cardiovascular disease and all-cause mortality, could play a role in the prognosis and quality of life of this population. Several studies using a variety of indices to assess arterial stiffness have tried to address the potential utility of arterial function assessment in the case of aortic stenosis. Importantly, reliable data identify a prognostic role of arterial biomarkers in aortic stenosis and stress their possible use to optimize timing and method of treatment. This review aims at summarizing the existing knowledge on the interplay between the heart and the vessels in the presence of degenerative aortic stenosis, prior, upon and after interventional management. Further, it discusses the evidence supporting the potential clinical application of arterial biomarkers for the assessment of progression, severity, management and prognosis of aortic stenosis.

Neuromuscular diseases (NMD) encompass a broad spectrum of diseases with variable type of cardiac involvement and there is lack of clinical data on Cardiovascular Magnetic Resonance (CMR) phenotypes or even prognostic value of CMR in NMD. We explored the diagnostic and prognostic value of CMR in NMD-related cardiomyopathies. The study included retrospective analysis of a cohort of 111 patients with various forms of NMD; mitochondrial: n = 14, Friedreich’s ataxia (FA): n = 27, myotonic dystrophy: n = 27, Becker/Duchenne’s muscular dystrophy (BMD/DMD): n = 15, Duchenne’s carriers: n = 6, other: n = 22. Biventricular volumes and function and myocardial late gadolinium enhancement (LGE) pattern and extent were assessed by CMR. Patients were followed-up for the composite clinical endpoint of death, heart failure development or need for permanent pacemaker/intracardiac defibrillator. The major NMD subtypes, i.e. FA, mitochondrial, BMD/DMD, and myotonic dystrophy had significant differences in the incidence of LGE (56%, 21%, 62% & 30% respectively, chi2 = 9.86, p = 0.042) and type of cardiomyopathy phenotype (chi2 = 13.8, p = 0.008), extent/pattern (p = 0.006) and progression rate of LGE (p = 0.006). In survival analysis the composite clinical endpoint differed significantly between NMD subtypes (p = 0.031), while the subgroup with LGE + and LVEF

Sexual health has a fundamental role in overall health and well-being, and a healthy and dynamic sex life can make an important contribution to a good quality of life. Sexual dysfunction, and especially erectile dysfunction (ED) in men, is highly prevalent in patients with cardiovascular disease (CVD). CVD and ED have shared risk factors and pathophysiological links, such as endothelial dysfunction, inflammation and low plasma testosterone levels. ED has been shown to be an independent and early harbinger of future CVD events, providing an important window to initiate preventive measures. Therefore, screening and diagnosing ED is essential for the primary and secondary prevention of CVD because the assessment of ED offers an easy and low-cost prognostic tool that is an alternative to other investigational cardiovascular biomarkers. Moreover, ED is a major contributing factor to the discontinuation of, or poor adherence to, cardiovascular therapy. Cardiovascular drugs have divergent effects on erectile function, with diuretics and β-blockers having the worst profiles, and renin-angiotensin-aldosterone system inhibitors and nebivolol having the best profiles. Pharmacological treatment of ED has an equivocal effect on the risk of CVD, suggesting a complex interaction between ED and drugs for CVD. In this Review, we discuss how sexual function could be incorporated into the patient history taken by physicians treating individuals with CVD, not merely as part of the diagnostic work-up but as a means to pursue tangible and essential benefits in quality of life and cardiovascular outcomes.

Background Abnormal cellular lipid metabolism appears to underlie SARS-CoV-2 cytotoxicity and may involve inhibition of peroxisome proliferator activated receptor alpha (PPARα). Fenofibrate, a PPAR-α activator, modulates cellular lipid metabolism. Fenofibric acid has also been shown to affect the dimerization of angiotensin-converting enzyme 2, the cellular receptor for SARS-CoV-2. Fenofibrate and fenofibric acid have been shown to inhibit SARS-CoV-2 replication in cell culture systems in vitro. Methods We randomly assigned 701 participants with COVID-19 within 14 days of symptom onset to 145 mg of fenofibrate (nanocrystal formulation with dose adjustment for renal function or dose-equivalent preparations of micronized fenofibrate or fenofibric acid) vs. placebo for 10 days, in a double-blinded fashion. The primary endpoint was a ranked severity score in which participants were ranked across hierarchical tiers incorporating time to death, duration of mechanical ventilation, oxygenation parameters, subsequent hospitalizations and symptom severity and duration. ClinicalTrials.gov registration: NCT04517396. Findings: Mean age of participants was 49 ± 16 years, 330 (47%) were female, mean BMI was 28 ± 6 kg/m2, and 102 (15%) had diabetes mellitus. A total of 41 deaths occurred. Compared with placebo, fenofibrate administration had no effect on the primary endpoint. The median (interquartile range [IQR]) rank in the placebo arm was 347 (172, 453) vs. 345 (175, 453) in the fenofibrate arm (P = 0.819). There was no difference in various secondary and exploratory endpoints, including all-cause death, across randomization arms. These results were highly consistent across pre-specified sensitivity and subgroup analyses. Conclusion Among patients with COVID-19, fenofibrate has no significant effect on various clinically relevant outcomes.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cytotoxicity may involve inhibition of peroxisome proliferator-activated receptor alpha. Fenofibrate activates peroxisome proliferator-activated receptor alpha and inhibits SARS-CoV-2 replication in vitro. Whether fenofibrate can be used to treat coronavirus disease 2019 (COVID-19) infection in humans remains unknown. Here, we randomly assigned inpatients and outpatients with COVID-19 within 14 d of symptom onset to 145 mg of oral fenofibrate nanocrystal formulation versus placebo for 10 d, in a double-blinded fashion. The primary endpoint was a severity score whereby participants were ranked across hierarchical tiers incorporating time to death, mechanical ventilation duration, oxygenation, hospitalization and symptom severity and duration. In total, 701 participants were randomized to fenofibrate (n = 351) or placebo (n = 350). The mean age of participants was 49 ± 16 years, 330 (47%) were female, mean body mass index was 28 ± 6 kg/m

The assumption that light cigarette smoking, meaning smoking one to five cigarettes per day, is not so harmful has been dissipated by several studies. Regardless of the quantity of tobacco cigarettes, smoking remains a leading risk factor for the development and progression of cardiovascular diseases. Smoke is a mixture of several toxic chemicals, such as nicotine, carbon monoxide, and oxidants, implicated in the pathogenesis of cardiovascular and pulmonary diseases. Despite anti-smoking campaigns, a misconception concerning “safe smoking” still exists. The purpose of this literature review is to highlight the deleterious effect of light cigarette smoking and claim the consensus that there is no safe smoking.

The study of arterial properties in patients with aortic valve stenosis who undergo transcatheter aortic valve implantation (TAVI) remains challenging and results so far seem equivocal. We sought to investigate the acute and long-term effect of TAVI on arterial stiffness and wave reflections.We enrolled 90 patients (mean age 80.2 ± 8.1 years, 50% males) with severe symptomatic aortic stenosis undergoing TAVI. Arterial stiffness was assessed by carotid-femoral and brachial-ankle pulse wave velocity (cfPWV and baPWV). Augmentation index corrected for heart rate (AIx@75), central pressures and subendocardial viability ratio (SEVR) were assessed with arterial tonometry. Measurements were conducted at baseline, after TAVI and at 1 year.Immediately after TAVI there was an increase in arterial stiffness (7.5 ± 1.5 m/s vs 8.4 ± 1.7 m/s, p = .001 for cfPWV and 1773 ± 459 vs 2383 ± 645 cm/s, p .001 for baPWV) that was retained at 1 year (7.5 ± 1.5 m/s vs 8.7 ± 1.7 m/s, p .001 and 1773 ± 459 cm/s vs 2286 ± 575, p .001). Post-TAVI we also observed a decrease in AIx@75 (32.2 ± 12.9% vs 27.9 ± 8.4%, p = .016) that was attenuated 1 year later (32.2 ± 12.9% vs 29.8 ± 9.1%, p = .38), and an increase in SEVR (131.2 ± 30.0% vs 148.4 ± 36.1%, p = .002), which remained improved at 1 year (131.2 ± 30.0% vs 146.0 ± 32.2%, p = .01).After TAVI the arterial system exhibits an increase of stiffness in response to the acute relief of the obstruction, which is retained in the long term.

The main pericardial syndromes include acute and recurrent pericarditis, constrictive pericarditis and chronic pericardial effusion in the absence of overt inflammation. Despite recent advances in pericardial syndromes, certain clinical scenarios depict remarkable peculiarities and their management is often challenging for the clinician. Acute pericarditis is the most common pericardial disease and in most instances is accompanied by pericardial effusion. On the other hand, pericardial effusion may appear as a separate clinical entity occasionally characterized by absence of inflammatory markers elevation. In cases that effusions are accompanied by C-reactive protein (CRP) elevation, the administration of empiric anti-inflammatory treatment as in acute pericarditis, is the guidelines recommended approach. Conversely, the optimal management of patients with pericardial effusions in the absence of clinical or subclinical inflammation (as depicted by CRP levels and cardiac magnetic resonance findings), is not supported by solid evidence. Patients with chronic pericardial effusions should be followed in specialized centers according to tailored timelines, based on the specific clinical scenarios which should take into account etiology, effusion size, disease duration and stability as regards symptoms and effusion volume. Patients should also be advised to seek medical care at any time if symptoms like chest pain, dyspnea and fatigue should appear.

Background There is evidence that metabolic disease burden in lymphoma influences patient outcome. However, the impact of disease severity on the cardiovascular system is unknown. Objectives The aim of this study was to examine whether lymphoma is associated with arterial inflammation by investigating the relationship between disease metabolic burden and arterial fluorodeoxyglucose (FDG) uptake. Methods Sixty-two chemotherapy-naive patients with active Hodgkin's or non-Hodgkin's lymphoma were matched (2:1) to individual control groups of lymphoma patients previously treated and free of active disease. All groups underwent 18F-FDG position emission tomography-computed tomography imaging. Disease severity was quantified by metabolic tumor volume (MTV) and total lesion glycolysis corresponding to standardized uptake values (SUVs) ≥41% or ≥2.5 of the maximum SUV within lymphoma regions, and aortic FDG uptake was quantified through the target-to-background ratio (TBR). Inflammatory and disease severity biomarkers were also measured. Results MTV and total lesion glycolysis measurements were significantly correlated with inflammatory and disease biomarkers. Aortic TBR was higher in patients with active non-Hodgkin's lymphoma compared with control subjects (median difference 0.51; 95% confidence interval [CI]: 0.28 to 0.78; p < 0.001). Similarly, patients with active Hodgkin's lymphoma had higher values of aortic TBR compared with control subjects (median difference 0.31; 95% CI: 0.15 to 0.49; p < 0.001). In addition, aortic TBR was modestly increased in patients with stage III to IV disease compared with those with stage I to II disease (median aortic TBR: 2.23 [interquartile range: 2.01 to 2.54] vs. 2.06 [interquartile range: 1.83 to 2.27; p = 0.050). In multivariable analysis, aortic FDG uptake and MTV≥2.5 values were independently associated (β = 0.425; 95% CI: 0.189 to 0.662; p = 0.001; R2 = 0.208), as were aortic FDG uptake and MTV≥41% (β = 0.407; 95% CI: 0.167 to 0.649, p = 0.001; R2 = 0.191). Conclusions Aortic wall FDG uptake is related with disease severity indicative of a possible vascular effect of lymphoma. This work highlights a new potential role of molecular imaging in cardio-oncology for evaluating disease severity and its consequences on the vasculature.

The score based on the office systolic blood pressure, age, fasting blood glucose level, and estimated glomerular filtration rate (SAGE score) has been proposed as a useful marker to identify elevated values of carotid-femoral pulse wave velocity (PWV). The present cross-sectional study was conducted to examine whether the SAGE score is also a useful marker to identify subjects with elevated brachial-ankle PWV values in Japanese subjects with hypertension. We measured the brachial-ankle PWV and calculated the SAGE score in a total of 1019 employees of a Japanese company with hypertension and 817 subjects with hypertension derived from a multicenter study cohort. The analyses in this study were based on data from these two study groups as well as on a composite population of the two (n = 1836). The receiver operating characteristic curve analysis showed that the area under the curve to identify subjects with brachial-ankle PWV values of ≥1800 cm/s was over 0.70 in each of the three study groups. Even after adjustments, a SAGE score ≥7 had a significant odds ratio for identifying subjects with brachial-ankle PWV values ≥1800 cm/s in the 1836 study subjects from the composite occupational and multicenter study cohort (odds ratio = 2.1, 95% confidence interval = 1.4–3.0, P

Sexual health is an integral part of overall health, and an active and healthy sexual life is an essential aspect of a good life quality. Cardiovascular disease and sexual health share common risk factors (arterial hypertension, diabetes mellitus, dyslipidemia, obesity, and smoking) and common mediating mechanisms (endothelial dysfunction, subclinical inflammation, and atherosclerosis). This generated a shift of thinking about the pathophysiology and subsequently the management of sexual dysfunction. The introduction of phosphodiesterase type 5 inhibitors revolutionized the management of sexual dysfunction in men. This article will focus on erectile dysfunction and its association with arterial hypertension. This update of the position paper was created by the Working Group on Sexual Dysfunction and Arterial Hypertension of the European Society of Hypertension. This working group has been very active during the last years in promoting the familiarization of hypertension specialists and related physicians with erectile dysfunction, through numerous lectures in national and international meetings, a position paper, newsletters, guidelines, and a book specifically addressing erectile dysfunction in hypertensive patients. It was noted that erectile dysfunction precedes the development of coronary artery disease. The artery size hypothesis has been proposed as a potential explanation for this observation. This hypothesis seeks to explain the differing manifestation of the same vascular condition, based on the size of the vessels. Clinical presentations of the atherosclerotic and/or endothelium disease in the penile arteries might precede the corresponding manifestations from larger arteries. Treated hypertensive patients are more likely to have sexual dysfunction compared with untreated ones, suggesting a detrimental role of antihypertensive treatment on erectile function. The occurrence of erectile dysfunction seems to be related to undesirable effects of antihypertensive drugs on the penile tissue. Available information points toward divergent effects of antihypertensive drugs on erectile function, with diuretics and beta-blockers possessing the worst profile and angiotensin receptor blockers and nebivolol the best profile.

Aims Cardiovascular magnetic resonance (CMR) is valuable for the detection of cardiac involvement in neuromuscular diseases (NMDs). We explored the value of 2D- and 3D-left ventricular (LV) myocardial strain analysis using feature-tracking (FT)-CMR to detect subclinical cardiac involvement in NMD. Methods and results The study included retrospective analysis of 111 patients with NMD; mitochondrial cytopathies (n = 14), Friedreich’s ataxia (FA, n = 27), myotonic dystrophy (n = 27), Becker/Duchenne’s muscular dystrophy (BMD/DMD, n = 15), Duchenne’s carriers (n = 6), or other (n = 22) and 57 age- and sex-matched healthy volunteers. Biventricular volumes, myocardial late gadolinium enhancement (LGE), and LV myocardial deformation were assessed by FT-CMR, including 2D and 3D global circumferential strain (GCS), global radial strain (GRS), global longitudinal strain (GLS), and torsion. Compared with the healthy volunteers, patients with NMD had impaired 2D-GCS (P < 0.001) and 2D-GRS (in the short-axis, P < 0.001), but no significant differences in 2D-GRS long-axis (P = 0.101), 2D-GLS (P = 0.069), or torsion (P = 0.122). 3D-GRS, 3D-GCS, and 3D-GLS values were all significantly different to the control group (P < 0.0001 for all). Especially, even NMD patients without overt cardiac involvement (i.e. LV dilation/hypertrophy, reduced LVEF, or LGE presence) had significantly impaired 3D-GRS, GCS, and GLS vs. the control group (P < 0.0001). 3D-GRS and GCS values were significantly associated with the LGE presence and pattern, being most impaired in patients with transmural LGE. Conclusions 3D-FT CMR detects subclinical cardiac muscle disease in patients with NMD even before the development of replacement fibrosis or ventricular remodelling which may be a useful imaging biomarker for early detection of cardiac involvement.

Accumulating evidence considers psoriasis a systemic inflammatory disorder that is associated with comorbidities such as psoriatic arthritis, cardiovascular disease, and metabolic syndrome. Although the precise pathogenetic links between psoriasis and atherosclerosis warrants further investigation, it is believed that chronic systemic inflammation along with the T helper (Th)-1 and Th17 polarization are associated with endothelial dysfunction and subsequent acceleration of atherosclerosis. Considering the above, several studies have evaluated if optimal control of the inflammation in psoriasis by inhibiting interleukins targeting the Interleukin (IL)-23/Th17 axis could subsequently reduce the atherosclerotic process during anti-psoriatic treatment by using a variety of surrogate markers of subclinical atherosclerosis. This systematic review summarizes current knowledge on the pathogenetic mechanisms and diagnostic evaluation of atherosclerosis in the context of psoriasis and provides a systematic review of the literature on the impact of treatment with biologics targeting the IL-23/Th17 axis on subclinical atherosclerosis in patients with plaque psoriasis and/or psoriatic arthritis.

Despite the remarkable development of the medical industry in the current era, herbal products with therapeutic potentials arise as attractive alternative treatments. Consequently, Chios mastiha, a natural, aromatic resin obtained from the trunk and brunches of the mastic tree, has recently gained increasing scientific interest due to its multiple beneficial actions. Chios mastiha is being exclusively produced on the southern part of Chios, a Greek island situated in the northern Aegean Sea, and its therapeutic properties have been known since Greek antiquity. There is now substantial evidence to suggest that mastiha demonstrates a plethora of favorable effects, mainly attributed to the anti-inflammatory and anti-oxidative properties of its components. The main use of mastiha nowadays, however, is for the production of natural chewing gum, although an approval by the European Medicines Agency for mild dyspeptic disorders and for inflammations of the skin has been given. The aim of this article is to summarize the most important data about the therapeutic actions of Chios mastiha and discuss future fields for its medical application.