Mihnea Casian

Objectives: The study aimed to evaluate differences in conventional, tissue Doppler imaging (TDI) and speckle-tracking echocardiographic (STE) parameters of all cardiac chambers between SSc patients and healthy controls. Methods: A study search strategy based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) was performed. MEDLINE, Scopus and Web of Science were searched using the following keywords: “speckle tracking”, “global strain”, “longitudinal strain”, “circumferential strain”, “radial strain”, “atrial strain”, “right ventricular strain”, or “left ventricular strain” and “systemic sclerosis”. Primary pooled analyses were performed on each cardiac parameter independently to determine the weighted mean difference (WMD) between SSc and controls. Further independent subgroup analyses were performed to compare symptomatic vs asymptomatic SSc and diffuse vs limited SSc. Results: The systematic review and meta-analysis included 41 case–control eligible reports studies with a pooled sample size of 2497 SSc cases and 1439 controls. Significant weighted mean differences (WMD) between SSc patients and healthy controls were identified in septal S’ wave (WMD 0.343 cm/s, CI [− 0.540–0.145], I²: 36%, p = 0.001), lateral S’ wave (WMD 0.795 cm/s, CI [− 1.394–0.197], I²: 0%, p = 0.009), tricuspid S’ wave (WMD 1.137 cm/s, CI [− 1.784–0.489], I²: 84%, p = 0.001), septal e’ wave (WMD 1.398 cm/s, CI [− 2.272–0.523], I²: 82%, p = 0.002) and lateral e’ wave (WMD 3.545 cm/s, CI [− 4.990–2.100], I²: 71%, p < 0.001) velocities. STE parameters were attenuated in patients with SSc, with impairment of left ventricular global longitudinal (WMD 2.765%, CI [− 3.482–2.049], I²: 91%, p < 0.001), circumferential (WMD 3.145%, CI [− 4.181–2.109], I²: 79%, p < 0.001), and radial (WMD 4.044%, CI [− 6.199–1.889], I²: 0%, p < 0.001) strain, right ventricular free wall (WMD 4.492%, CI [− 6.048–2.937], I²: 76%, p < 0.001) and right ventricular global longitudinal strain (WMD 2.843%, CI [− 3.290–2.396], I²: 32%, p < 0.001), as well as left (WMD − 8.317%, CI [− 11.873–4.761], I²: 82%, p < 0.001) and right (WMD 7.346%, CI [− 10.536–4.156], I²: 26%, p < 0.001) atrial reservoir strain. Conclusion: SSc is associated with significantly impaired cardiac function and mechanics compared to healthy individuals, even in the absence of symptoms or pulmonary hypertension. Graphical

Introduction: CPVT is a rare inherited channelopathy which predisposes patients to malignant ventricular arrhythmias during exercise or stress. Although exceptionally rare, the diagnosis can be made in individuals over 40 years. Case presentation: A 58-year-old male with persistent atrial fibrillation was evaluated for exercise prescription. He was keen on low-intensity skill sports and medium-intensity endurance sports. He reported no symptoms and had no relevant family history. The ECG showed atrial fibrillation without other abnormalities. The transthoracic echocardiogram demonstrated severe left atrial dilatation but nothing else of note. The exercise test revealed a poorly controlled ventricular rate with effort, with frequent monomorphic PVC and a 4-beat NSVT. The CTCA and CMR excluded significant coronary artery disease or an underlying cardiomyopathy. The bisoprolol dose was increased, and the patient was advised to limit his training to moderate-intensity exercise. In the meantime, the patient’s 25-year-old daughter suffered a sudden cardiac arrest and was found to harbor a pathogenic RYR2 mutation, later identified in our patient through predictive genetic testing. The patient was reassessed considering the genetic result. An exercise test revealed bi-directional PVCs. He was switched on a non-selective beta-blocker. Specific exercise prescription and lifestyle changes were discussed. Conclusion: Genetic testing in CPVT is crucial for diagnosis and prognosis of affected individuals, as well as for identifying family members at risk, even in the absence of a characteristic phenotype.

Extraglandular manifestations (EGMs) in primary Sjogren’s syndrome (pSS) represent the clinical expression of the systemic involvement in this disease. EGMs are characterized by a wide heterogeneity; virtually any organ or system can be affected, with various degrees of dysfunction. The existing gaps of knowledge in this complex domain of extraglandular extension in pSS need to be overcome in order to increase the diagnostic accuracy of EGMs in pSS. The timely identification of EGMs, as early as from subclinical stages, can be facilitated using highly specific biomarkers, thus preventing decompensated disease and severe complications. To date, there is no general consensus on the diagnostic criteria for the wide range of extraglandular involvement in pSS, which associates important underdiagnosing of EGMs, subsequent undertreatment and progression to severe organ dysfunction in these patients. This review article presents the most recent basic and clinical science research conducted to investigate pathogenic mechanisms leading to EGMs in pSS patients. In addition, it presents the current diagnostic and treatment recommendations and the trends for future therapeutic strategies based on personalized treatment, as well as the latest research in the field of diagnostic and prognostic biomarkers for extraglandular involvement in pSS.

In the ever evolving landscape of systemic immune mediated diseases, an increased awareness regarding the associated cardiovascular system impairment has been noted in recent years. Even though primary Sjögren’s Syndrome (pSS) is one of the most frequent autoimmune diseases affecting middle-aged individuals, the cardiovascular profile of this specific population is far less studied, at least compared to other autoimmune diseases. Traditional cardiovascular risk factors and disease specific risk factors are inextricably intertwined in this particular case. Therefore, the cardiovascular risk profile in pSS is a multifaceted issue, sometimes difficult to assess. Furthermore, in the era of multimodality imaging, the diagnosis of subclinical myocardial and vascular damage is possible, with recent data pointing that the prevalence of such involvement is higher in pSS than in the general population. Nevertheless, when approaching patients with pSS in terms of cardiovascular diseases, clinicians are often faced with the difficult task of translating data from the literature into their everyday practice. The present review aims to synthesize the existing evidence on pSS associated cardiovascular changes in a clinically relevant manner.

Background and Objectives: Romania has one of the highest prevalence of hepatitis B virus (HBV) infection in human immunodeficiency virus (HIV) patients, mostly in those parenterally infected during childhood; nevertheless, there are scarce data on the virological profile of co-infection. The objective of this study was to assess the prevalence of HBV genotypes and antiviral resistance-associated mutations (RAMs) in these co-infected patients, in order to monitor the viral factors associated with the evolution of liver disease. Materials and Methods: HBV genotypes and RAMs were detected using nested PCR and line probe assays (INNO-LiPA HBV genotyping assay, and INNO-LiPA HBV DR v2, Innogenetics). Results: Out of 117 co-infected patients, 73.5% had detectable HBV-DNA, but only 38.5% presented an HBV viral load >1000 IU/mL. HBV genotype A was present in 66.7% of the cases and was dominant in patients parenterally infected during early childhood, who experienced multiple treatment regimens, with a mean therapy length of 15.25 years, and present numerous mutations associated with lamivudine (LAM) resistance, but very rarely active liver disease. HBV genotype D was detected in 33.3% of the cases, mostly in recently diagnosed injecting drug users who are treatment naïve, but, nevertheless, present RAMs in 63.5% of the cases, suggesting transmitted drug resistance, and display more frequently advanced liver fibrosis (36.1% vs. 12.3%; p = 0.033). The most frequently encountered RAMs are M204V/I: 48.8%, L180M: 33.3%, L80V: 28.8%, and V173L: 42.2%. There are no significant differences in the distribution of RAMs in patients infected with different HBV genotypes, except for the L80V and N236T mutations, which were more frequently found in HBV genotype A infections (p = 0.032 and p = 0.004, respectively). Conclusions: HBV genotypes A and D are the only genotypes present in HIV–HBV co-infected patients from Romania, with different distributions according to the infection route, and are frequently associated with multiple RAMs, conferring extensive resistance to LAM.

The medical therapy of heart failure (HF) has been traditionally based on inhibiting the main pathophysiologic mechanisms: the adrenergic and renin-angiotensin-aldosterone systems. Introducing the therapeutical triad of beta-blockers, angiotensin converting enzyme inhibitors and mineralocorticoid receptor antagonists in the treatment of HF patients almost 40 years ago marked an important step since they were not only addressing the symptoms of HF, but also the prognosis and life- expectancy of these patients. Although many discoveries have been made in the past years, no other therapeutic class was able to increase survival among HF patients, until recently, when th SA e benefits of modulating the natriuretic peptide system were brought to the attention of the scientific community. Increasing the levels of natriuretic peptides with Sacubitril/ Valsartan (SV) led to several benefits for the reduced ejection fraction HF population, including less long and short term complications, increased survival and a reduced symptom burden. As this article is being written, it is estimated that more than 2.8 million patients are being treated with SV(1). Therefore, SV is an important and validated therapy for HF patients and internists should be aware of its indications, benefits and management in clinical practice.