Traditional and emerging biomarkers in asymptomatic left ventricular dysfunction\u2014promising non-coding rnas and exosomes as biomarkers in early phases of cardiac damage

Heart failure (HF) is one of the major causes of morbidity and mortality worldwide and represents an escalating problem for healthcare systems. The identification of asymptomatic patients with underlying cardiac subclinical disease would create an opportunity for early intervention and prevention of symptomatic HF. Traditional biomarkers are very useful as diagnostic and prognostic tools in the cardiovascular field; however, their application is usually limited to overt cardiac disease. On the other hand, a growing number of studies is investigating the diagnostic and prognostic potential of new biomarkers, such as micro-RNAs (miRNA), long non-coding RNAs, and exosome cargo, because of their involvement in the early phases of cardiac dysfunction. Unfor-tunately, their use in asymptomatic phases remains a distant goal. The aim of this review is to gather the current knowledge of old and novel biomarkers in the early diagnosis of cardiac dysfunction in asymptomatic individuals

What the cardiologist needs to consider in the management of oncologic patients with stemi-like syndrome; A case report and literature review

In pre-hospital care, an accurate and quick diagnosis of ST-segment elevation myocardial infarction (STEMI) is imperative to promptly kick-off the STEMI network with a direct transfer to the cardiac catheterization laboratory (cath lab) in order to reduce myocardial infarction size and mortality. Aa atherosclerotic plaque rupture is the main mechanism responsible for STEMI. However, in a small percentage of patients, emergency coronarography does not reveal any significant coronary stenosis. The fluoropyrimidine agents such as 5-Fluorouracil (5-FU) and capecitabine, widely used to treat gastrointestinal, breast, head and neck cancers, either as a single agent or in combination with other chemotherapies, can cause potentially lethal cardiac side effects. Here, we present the case of a patient with 5-FU cardiotoxicity resulting in an acute coronary syndrome (ACS) with recurrent episodes of chest pain and ST-segment elevation.. Our case report highlights the importance of widening the knowledge among cardiologists of the side effects of chemotherapeutic drugs, especially considering the rising number of cancer patients around the world and that fluoropyrimidines are the main treatment for many types of cancer, both in adjuvant and advanced settings

COVID-19-Related Myocarditis: Are We There Yet? A Case Report of COVID-19-Related Fulminant Myocarditis

There is increasing evidence of cardiac involvement in COVID-19 cases, with a broad range of clinical manifestations spanning from acute life-threatening conditions such as ventricular dysrhythmias, myocarditis, acute myocardial ischemia and pulmonary thromboembolism to long-term cardiovascular sequelae. In particular, acute myocarditis represents an uncommon but frightening complication of SARS-CoV-2 infection. Even if many reports of SARS CoV-2 myocarditis are present in the literature, the majority of them lacks histological confirmation of cardiac injury. Here, we report a case of a young lady, who died suddenly a few days after testing positive for SARS-CoV-2, whose microscopic and genetics features suggested a direct cardiac involvement compatible with fulminant myocarditis

Prospective Evaluation of Clinico-Pathological Predictors of Postoperative Atrial Fibrillation

Background: Postoperative atrial fibrillation (POAF) occurs in 30% to 50% of patients undergoing cardiac surgery and is associated with increased morbidity and mortality. Prospective identification of structural/molecular changes in atrial myocardium that correlate with myocardial injury and precede and predict risk of POAF may identify new molecular pathways and targets for prevention of this common morbid complication. Methods: Right atrial appendage samples were prospectively collected during cardiac surgery from 239 patients enrolled in the OPERA trial (Omega-3 Fatty Acids for Prevention of Post-Operative Atrial Fibrillation), fixed in 10% buffered formalin, and embedded in paraffin for histology. We assessed general tissue morphology, cardiomyocyte diameters, myocytolysis (perinuclear myofibril loss), accumulation of perinuclear glycogen, interstitial fibrosis, and myocardial gap junction distribution. We also assayed NT-proBNP (N-terminal pro-B-type natriuretic peptide), hs-cTnT, CRP (C-reactive protein), and circulating oxidative stress biomarkers (F2-isoprostanes, F3-isoprostanes, isofurans) in plasma collected before, during, and 48 hours after surgery. POAF was defined as occurrence of postcardiac surgery atrial fibrillation or flutter of at least 30 seconds duration confirmed by rhythm strip or 12-lead ECG. The follow-up period for all arrhythmias was from surgery until hospital discharge or postoperative day 10. Results: Thirty-five percent of patients experienced POAF. Compared with the non-POAF group, they were slightly older and more likely to have chronic obstructive pulmonary disease or heart failure. They also had a higher European System for Cardiac Operative Risk Evaluation and more often underwent valve surgery. No differences in left atrial size were observed between patients with POAF and patients without POAF. The extent of atrial interstitial fibrosis, cardiomyocyte myocytolysis, cardiomyocyte diameter, glycogen score or Cx43 distribution at the time of surgery was not significantly associated with incidence of POAF. None of these histopathologic abnormalities were correlated with levels of NT-proBNP, hs-cTnT, CRP, or oxidative stress biomarkers. Conclusions: In sinus rhythm patients undergoing cardiac surgery, histopathologic changes in the right atrial appendage do not predict POAF. They also do not correlate with biomarkers of cardiac function, inflammation, and oxidative stress

Arrhythmias in Dilated Cardiomyopathy: Diagnosis and Treatment

In patients with dilated cardiomyopathy (DCM), it is possible to find a broad range of bradyrhythmias and tachyarrhythmias. Bradyrhythmias and supraventricular arrhythmias can frequently occur in some familial forms such as lamin A/C mutations. Nonsustained ventricular arrhythmias (VA) are observed in about 40% of patients with DCM, but their prognostic role is not clear, and conflicting data have been published in the last 30 years. Multiple mechanisms can explain atrial and ventricular tachyarrhythmias in DCM. Reentry is associated with slow conduction across surviving muscle bundles within regions of interstitial fibrosis, but other mechanisms can be involved, as nonuniform anisotropy of impulse propagation, ion channel dysfunction, and reduced gap junction function

From brain to heart: Possible role of amyloid-\u3b2 in ischemic heart disease and ischemia-reperfusion injury

Ischemic heart disease (IHD) is among the leading causes of death in developed countries. Its pathological origin is traced back to coronary atherosclerosis, a lipid-driven immuno-inflammatory disease of the arteries that leads to multifocal plaque development. The primary clinical manifestation of IHD is acute myocardial infarction (AMI),) whose prognosis is ameliorated with optimal timing of revascularization. Paradoxically, myocardium re-perfusion can be detrimental because of ischemia-reperfusion injury (IRI), an oxidative-driven process that damages other organs. Amyloid-\u3b2 (A\u3b2) plays a physiological role in the central nervous system (CNS). Alterations in its synthesis, concentration and clearance have been connected to several pathologies, such as Alzheimer\u2019s disease (AD) and cerebral amyloid angiopathy (CAA). A\u3b2 has been suggested to play a role in the pathogenesis of IHD and cerebral IRI. The purpose of this review is to summarize what is known about the pathological role of A\u3b2 in the CNS; starting from this evidence, we will illustrate the role played by A\u3b2 in the development of coronary atherosclerosis and its possible implications in the pathophysiology of IHD and myocardial IRI. Better elucidation of A\u3b2\u2019s contribution to the molecular pathways underlying IHD and IRI could be of great help in developing new therapeutic strategies. \ua9 2020 by the authors

Intraoperative Neuromonitoring of the External Branch of the Superior Laryngeal Nerve During Thyroid Surgery

Thyroid gland surgeries are among the most common surgical interventions worldwide and are considered by many surgeons as a relatively easy and safe procedure. But the number of complications still remains significant with unacceptable and unpleasant consequences for the patients. Among them, the most significant are postoperative hypoparathyroidism and the injuries of the laryngeal nerves - the recurrent laryngeal nerve (RLN) and the external branch of the superior laryngeal nerve (EBSLN). Nowadays, the surgical anatomy of the recurrent laryngeal nerves and the surgical approach to them are described in detail in the medical literature and their damages are perhaps the most known and discussed complications. EBSLN injury leads to paralysis of the cricothyroid muscle (CTM) and often remains unseen due to a lack of clear laryngoscopic markers. The main postoperative symptoms are accompanied mostly by qualitative voice disturbances of the patients. A relatively new method for timely assessment of the risk of iatrogenic lesions of the laryngeal nerves in thyroid surgery is the intraoperative neuromonitoring (IONM). The method emerged as the gold standard of care for prevention of RLN, and lately its application on EBSLN is subject of detailed analysis. This creates a need to assess the method and develop a friendly practice system for its clinical application

The peculiar role of vitamin D in the pathophysiology of cardiovascular and neurodegenerative diseases

Vitamin D is a hormone with both genomic and non-genomic actions. It exerts its activity by binding vitamin D receptor (VDR), which belongs to the superfamily of nuclear receptors and ligand-activated transcription factors. Since VDR has been found in various tissues, it has been estimated that it regulates approximately 3% of the human genome. Several recent studies have shown pleiotropic effects of vitamin D in various processes such as cellular proliferation, differentiation, DNA repair and apoptosis and its involvement in different pathophysiological conditions as inflammation, diabetes mellitus, and anemia. It has been suggested that vitamin D could play an important role in neurodegenerative and cardiovascular disorders. Moderate to strong associations between lower serum vitamin D concentrations and stroke and cardiovascular events have been identified in different analytic approaches, even after controlling for traditional demographic and lifestyle covariates. The mechanisms behind the associations between vitamin D and cerebrovascular and cardiologic profiles have been widely examined both in animal and human studies. Optimization of vitamin D levels in human subjects may improve insulin sensitivity and beta-cell function and lower levels of inflammatory markers. Moreover, it has been demonstrated that altered gene expression of VDR and 1,25D3-membrane-associated rapid response steroid-binding (1,25D3-MARRS) receptor influences the role of vitamin D within neurons and allows them to be more prone to degeneration. This review summarizes the current understanding of the molecular mechanisms underlying vitamin D signaling and the consequences of vitamin D deficiency in neurodegenerative and cardiovascular disorders

Vitamin D and cardiovascular diseases

Vitamin D is a hormone with pleiotropic effects; it controls calcium homeostasis, immune response, hemodynamic wall stress (by inhibiting Renin Angiotensin Aldosterone System, RAAS, and modulating the endothelial function) and inflammation. In the last decade, numerous studies have focused on the role of vitamin D levels in the setting of cardiovascular disease. In particular, it has been shown that insufficient Vitamin D levels are frequently observed among patients with cardiovascular disease. Hypovitaminosis D activates the renin angiotensin system, causes endothelial dysfunction, reduces cardiomyocyte contractility and is associated with adverse left ventricular remodelling after myocardial infarction. Also, low Vitamin D levels are associated with worse outcome. However, there is still no evidence in supporting an extended use of oral hormone supplementation. Two big epidemiological studies including patients from general practice suggested a U-shape correlation between Vitamin D levels and survival; furthermore, we observed similar results in survivors after myocardial infarction; the prognosis of patients with Vitamin D-i.e., 25-(OH) D-levels 30 ng/mL was markedly worse than the prognosis of patients with levels between 10 and 30 ng/mL. Probably, the new therapeutic strategy should consider the non-linear relationship that exists between Vitamin D levels and the prognosis and should provide careful measurements of the blood levels of this hormone