Classic endocrine disorders: implications for cardiovascular disease

Chronic underproduction or autonomous oversecretion of hormone by endocrine glands has implications for the development and progression of cardiovascular disease. Hormonal effects on the vasculature may be direct, for example, tachycardia and atrial arrhythmias in hyperthyroidism, or mediated indirectly via adverse profiles of one or more major cardiovascular risk factors, for example, arterial hypertension in Conn's syndrome. The timescale of vascular effects may be relatively rapid, for example, resting tachycardia or atrial fibrillation precipitated by hyperthyroidism, or long-term, for example, atherosclerosis associated with acromegaly or hypopituitarism of long duration. The COVID-19 pandemic has highlighted clinically important interactions between the endocrine, metabolic, and cardiovascular systems. Endocrinologists and cardiologists will often need to collaborate closely in the management of patients with endocrine-associated vascular disease. © 2023 Elsevier Inc. All rights reserved.

Acute Coronary Syndrome during the Pandemic New Coronavirus Infection.

The experience of managing patients with COVID-19 around the world has shown that, although respiratory symptoms predominate during the manifestation of infection, then many patients can develop serious damage to the cardiovascular system. However, coronary artery disease (CHD) remains the leading cause of death worldwide. The purpose of the review is to clarify the possible pathogenetic links between COVID-19 and acute coronary syndrome (ACS), taking into account which will help to optimize the management of patients with comorbid pathology. Among the body's responses to SARS-CoV-2 infection, which increase the likelihood of developing ACS, the role of systemic inflammation, the quintessence of which is a "cytokine storm" that can destabilize an atherosclerotic plaque is discussed. Coagulopathy, typical for patients with Covid-19, is based on immunothrombosis, caused by a complex interaction between neutrophilic extracellular traps and von Willebrandt factor in conditions of systemic inflammation. The implementation of a modern strategy for managing patients with ACS, focused on the priority of percutaneous interventions (PCI), during a pandemic is experiencing great difficulties due to the formation of time delays before the start of invasive procedures due to the epidemiological situation. Despite this, the current European, American and Russian recommendations for the management of infected patients with ACS confirm the inviolability of the position of PCI as the first choice for treating patients with ACS and the undesirability of replacing invasive treatment with thrombolysis.Copyright © 2023 Stolichnaya Izdatelskaya Kompaniya. All rights reserved.

Barriers and shortcomings in access to cardiovascular management and prevention for familial hypercholesterolemia during the COVID-19 pandemic.

Familial hypercholesterolemia (FH) is a hereditary condition caused by mutations in the lipid pathway. The goal in managing FH is to reduce circulating low-density lipoprotein cholesterol and, therefore, reduce the risk of developing atherosclerotic cardiovascular disease (ASCVD). Because FH patients were considered high risk groups due to an increased susceptible for contracting COVID-19 infection, we hypothesized whether the effects of the pandemic hindered access to cardiovascular care. In this review, we conducted a literature search in databases Pubmed/Medline and ScienceDirect. We included a comprehensive analysis of findings from articles in English related and summarized the effects of the pandemic on cardiovascular care through direct and indirect effects. During the COVID-19 pandemic, FH patients presented with worse outcomes and prognosis, especially those that have suffered from early ASCVD. This caused avoidance in seeking care due to fear of transmission. The pandemic severely impacted consultations with lipidologists and cardiologists, causing a decline in lipid profile evaluations. Low socioeconomic communities and ethnic minorities were hit the hardest with job displacements and lacked healthcare coverage respectively, leading to treatment nonadherence. Lock-down restrictions promoted sedentary lifestyles and intake of fatty meals, but it is unclear whether these factors attenuated cardiovascular risk in FH. To prevent early atherogenesis in FH patients, universal screening programs, telemedicine, and lifestyle interventions are important recommendations that could improve outcomes in FH patients. However, the need to research in depth on the disproportionate impact within different subgroups should be the forefront of FH research.

SARS-CoV-2 reinfection: Adding insult to dysfunctional endothelium in patients with atherosclerotic cardiovascular disease.

In this short narrative review, we aim at defining the pathophysiological role endothelial dysfunction in the observed COVID-19-associated rise in risk of cardiovascular disease. Variants of the SARS-CoV-2 virus have caused several epidemic waves of COVID-19, and the emergence and rapid spread of new variants and subvariants are likely. Based on a large cohort study, the incidence rate of SARS-CoV-2 reinfection is about 0.66 per 10 000 person-weeks. Both the first infection and reinfection with SARS-CoV-2 increase cardiac event risk, particularly in vulnerable patients with cardiovascular risk factors and the accompanying systemic endothelial dysfunction. By worsening pre-existing endothelial dysfunction, both the first infection and reinfection with ensuing COVID-19 may turn the endothelium procoagulative and prothrombotic, and ultimately lead to local thrombus formation. When occurring in an epicardial coronary artery, the risk of an acute coronary syndrome increases, and when occurring in intramyocardial microvessels, scattered myocardial injuries will ensue, both predisposing the COVID-19 patients to adverse cardiovascular outcomes. In conclusion, considering weakened protection against the cardiovascular risk-enhancing reinfections with emerging new subvariants of SARS-CoV-2, treatment of COVID-19 patients with statins during the illness and thereafter is recommended, partly because the statins tend to reduce endothelial dysfunction.

Acute coronary syndrome: new realities in the era of the COVID-19 pandemic

Coronavirus infection (COVID-19) pandemic is a global health problem associated with high rates of morbidity and mortality. In this difficult time, the topic of acute coronary syndrome (ACS) is complicated by a number of clinically significant issues, such as COVID-induced myocardial damage, uncertainty of this emergency management, the need for a clear optimization of diagnostic and therapeutic measures, as well as ensuring maximum protection of medical personnel. In addition, there is a decrease in the number of hospitalizations for ACS worldwide, which is associated with the reluctance of patients to seek medical help and the redirection of medical resources in favor of combating the pandemic. Given that the primary pathophysiological mechanism of COVID-19 is a significant shift in blood coagulation rates, it is necessary to establish a relationship between this infection and an increased risk of acute coronary disease. The high risk of developing ACS associated with COVID-19 may be associated with atherosclerotic plaque rupture caused by endothelial cell damage, cytokine storms and the patient's inflammatory status. In this review will present aspects of the impact of the COVID-19 pandemic on the diagnosis, clinical course and treatment of ACS, as well as published data on the results of treatment of coronary syndrome in a pandemic.Copyright © 2022 by the Author(s).

Acute Coronary Syndrome during the Pandemic New Coronavirus Infection.

The experience of managing patients with COVID-19 around the world has shown that, although respiratory symptoms predominate during the manifestation of infection, then many patients can develop serious damage to the cardiovascular system. However, coronary artery disease (CHD) remains the leading cause of death worldwide. The purpose of the review is to clarify the possible pathogenetic links between COVID-19 and acute coronary syndrome (ACS), taking into account which will help to optimize the management of patients with comorbid pathology. Among the body's responses to SARS-CoV-2 infection, which increase the likelihood of developing ACS, the role of systemic inflammation, the quintessence of which is a "cytokine storm" that can destabilize an atherosclerotic plaque is discussed. Coagulopathy, typical for patients with Covid-19, is based on immunothrombosis, caused by a complex interaction between neutrophilic extracellular traps and von Willebrandt factor in conditions of systemic inflammation. The implementation of a modern strategy for managing patients with ACS, focused on the priority of percutaneous interventions (PCI), during a pandemic is experiencing great difficulties due to the formation of time delays before the start of invasive procedures due to the epidemiological situation. Despite this, the current European, American and Russian recommendations for the management of infected patients with ACS confirm the inviolability of the position of PCI as the first choice for treating patients with ACS and the undesirability of replacing invasive treatment with thrombolysis.Copyright © 2023 Stolichnaya Izdatelskaya Kompaniya. All rights reserved.

Successful Treatment of Subclavian Artery Thrombosis by Catheter-Based Thrombus Aspiration and Thrombolytic Therapy: A Case Report

Clinical Information Patient Initials or Identifier Number: BP4****/22 Relevant Clinical History and Physical Exam: A 55 Y / Female C/C : Pain, numbness, cold sensation & weakness of left upper limb for 2 hours. Risk Factor : Hypertension, diabetes mellitus O/E : Pale, cold and absent of radial, ulnar, brachial pulse of left upper limb. Muscle power 3/5 left side. So2 86%, BP undetectable. Right upper limb were normal. BP 160/90 mm of hg, pules : 112 b/min, RR : 26/min. Body Temperature 37.5 C [Formula presented] [Formula presented] Relevant Test Results Prior to Catheterization: CBC : WBC 7450, HB % 10.8 g/dl, ESR 20mm in 1st hour, Platelets : 262000, SARS Cov2 Antigen : Negative PT 14.3 sec, INR : 1.07 APTT : 32.4 sec. blood group: O positive Serum Creatinine : 1.1 mg/dl Plasma glucose 9.7 mmmol/l HIV Ab : Negative HBs Ag : Negative Anti-HCV : Negative Urine R/E : Normal lipid profile : Cholesterol 280mg/dl Vascular duplex ultrasound of left upper limb : A dilated echogenic thrombus had blocked the left subclaviav artery lumen. Relevant Catheterization Findings: Conventional angiography with the lowest amount of contrast agent through the right femoral artery, revealed that left subclavian artery thrombosis with total occlusion distal to Left internal mammary artery. [Formula presented] [Formula presented] [Formula presented] Interventional Management Procedural Step: A5Fr MPA catheter with side holes was negotiated through a right femoral sheath and was placed in the left subclavian artery. Initially thrombus aspiration was done with Eliminate aspiration catheter (TERUMO) with no success. Then suction was done with the MPA catheter itself with partial removal of thrombus. Then a 5Fr Pigtail catheter was placed inside the thrombus and kept in situ. For residual thrombus 250,000u of Inj. Streptokinase as a thrombolytic drug was given through the Pigtail catheter as bolus over 30 min. The maintenance dose 100,000 u per hour was given over 24 hours through the Pigtail catheter via infusion pump. After 24 hours of thrombolytic therapy, her pain was reduced, the left hand became slightly warm, and distal pulses were feebly palpable. Moreover, the skin colour returned to near normal with improvement of pallor. Bleeding was well controlled at the catheter site. Doppler sounds revealed partial improvement of arterial flow. After evaluation of partial improvement, a low dose 1000 iu per hour of heparin (UFH)was infused intravenously for 24 hours. After 48 hours, repeat angiography via the inserted catheter at the site did not reveal any atherosclerotic plaque and confirm the thrombosis-dissolution. The latter practice demonstrated a good blood flowto the left upper distal limb leaving a little thrombus in the superficial palmer arch. [Formula presented] [Formula presented] [Formula presented] Conclusion(s): Catheter-based thrombus aspiration and thrombolytic therapy is primarily reserved for patients with acute viable limb ischemia. As observed in the presented case, thrombus aspiration and thrombolytic therapy is recommended to be considered as an alternative therapeutic method for patients with arterial thrombosis due to the rapid response, shorter treatment time and lower cost, compared to common and sometimes unsuccessful therapies.Copyright © 2023

Beware of the Unexpected: Acute Coronary Thrombosis Following the Mildly Symptomatic COVID-19 Infection and Two Different Therapeutic Options

COVID-19 infection was declared a pandemic in March 2020 and is responsible for high morbidity and mortality around the globe. Although the most common clinical presentation is respiratory, cardiac complications are common and create new challenges for healthcare. We discuss two mildly symptomatic outpatients with COVID-19 presenting with acute ST-elevation myocardial infarction (STEMI) and high coronary thrombus burden without atherosclerotic plaque. Our report describes two different therapeutic approaches that illustrate the challenges encountered in the management of disseminated coronary thrombosis in patients with STEMI and COVID-19. Clinicians should be aware of the high pro-coagulant state caused by COVID-19, even in mildly symptomatic outpatients, and aggressive pharmacological therapy may be an effective alternative treatment option to percutaneous coronary intervention.Copyright © 2023, CKS.

The potential role of SARS-CoV-2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread.

Coronavirus disease 2019 (COVID-19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has been shown that SARS-CoV-2 infection-induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS-CoV-2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS-CoV-2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS-CoV-2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID-19 since coronary arteries are not initially and primarily targeted by SARS-CoV-2 due to low expression of angiotensin-converting enzyme 2 in coronary vessels. In conclusion, SARS-CoV-2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin-angiotensin system may aggravate underlying ACS or cause new-onset T2MI. As well, arrhythmias induced by anti-COVID-19 medications could worsen underlying ACS.

Familial Hypercholesterolemia Patients with COVID-19-Effective Cholesterol-Lowering Therapy is Urgent both during and after Infection

Heterozygous familial hypercholesterolemia (HeFH) patients are the prime example of subjects who are at high risk for both acute myocardial infarction (AMI) and ischemic stroke during, and post, SARS-CoV-2 infection. HeFH per se, if left untreated, results in premature clinical atherosclerosis often presenting in the fourth or fifth decade of life. The other concern in HeFH is endothelial dysfunction which is already evident from early childhood. In untreated HeFH patients, the severe hypercholesterolemia causes endothelial dysfunction from an early age, and as a result thereof, atherosclerotic lesions develop prematurely, particularly in the coronary arteries, and result in further endothelial dysfunction and inflammation in these critical segments of the arterial tree. As the pre-existing endothelial dysfunction in HeFH patients is most likely sensitive to further direct and indirect SARS-CoV-2 virus-dependent damage, we can infer that HeFH serves as an example of a comorbidity that predicts a poorer prognosis with COVID-19 infection. Indeed, a large US national database study showed that patients diagnosed with HeFH and SARS-CoV-2 infection had significantly increased Annualized Incidence Density Rates (AIDRs) of AMI when compared to matched HeFH controls not having been diagnosed with SARS-CoV-2 infection. Effective cholesterol lowering is essential for the prevention, or at least alleviation, of the detrimental effects of SARS-CoV-2 infection among HeFH patients. Due to the pre-existing subclinical or even clinical atherosclerotic cardiovascular disease in subjects with HeFH, cholesterol-lowering treatment needs to be continued or, better still, intensified during, and for an extended period post, SARS-CoV-2 infection.

An NMR-Based Model to Investigate the Metabolic Phenoreversion of COVID-19 Patients throughout a Longitudinal Study.

After SARS-CoV-2 infection, the molecular phenoreversion of the immunological response and its associated metabolic dysregulation are required for a full recovery of the patient. This process is patient-dependent due to the manifold possibilities induced by virus severity, its phylogenic evolution and the vaccination status of the population. We have here investigated the natural history of COVID-19 disease at the molecular level, characterizing the metabolic and immunological phenoreversion over time in large cohorts of hospitalized severe patients (n = 886) and non-hospitalized recovered patients that self-reported having passed the disease (n = 513). Non-hospitalized recovered patients do not show any metabolic fingerprint associated with the disease or immune alterations. Acute patients are characterized by the metabolic and lipidomic dysregulation that accompanies the exacerbated immunological response, resulting in a slow recovery time with a maximum probability of around 62 days. As a manifestation of the heterogeneity in the metabolic phenoreversion, age and severity become factors that modulate their normalization time which, in turn, correlates with changes in the atherogenesis-associated chemokine MCP-1. Our results are consistent with a model where the slow metabolic normalization in acute patients results in enhanced atherosclerotic risk, in line with the recent observation of an elevated number of cardiovascular episodes found in post-COVID-19 cohorts.

Cardiac Biomarkers and Risk Scores in Relation with History of Atherosclerotic Cardiovascular Disease in Patients Admitted with COVID-19: The Experience of an Eastern European Center.

BACKGROUND: Data regarding the combined prognostic role of biomarkers and risk scores in relation with the history of atherosclerotic cardiovascular disease (ASCVD) in COVID-19 patients are lacking. METHODS: The aim of this observational cohort study was to evaluate the combined prognostic value of N-terminal pro B-type natriuretic peptide (NT-pro BNP), troponin and risk scores in relation with ASCVD history in hospitalized COVID-19 patients. The primary composite endpoint was Intensive Care Unit (ICU) admission and death. RESULTS: From April 2020 to June 2022, 1066 consecutive COVID-19 patients with available biomarkers upon admission were included. During a median follow-up period of 12 days, 176 patients (16.5%) died. Independent predictors of ICU admission and death in patients with ASCVD were NT-pro BNP (HR 2.63; 95% CI, 1.65-4.18) and troponin (HR 1.51; 95% CI, 1.13-2.03). In patients without ASCVD, only NT-pro BNP was predictive for the primary endpoint (HR 1.66; 95% CI, 1.10-2.53). This remained significant after adjustment for other relevant covariates (HR 3.54; 95% CI, 1.98-6.33) in patients with ASCVD and in patients without ASCVD (HR 1.82; 95% CI, 1.02-3.26). CONCLUSIONS: These data showed the combined prognostic accuracy of NT-pro BNP and troponin in relation with ASCVD history for ICU admission and death in COVID-19 patients.

Human Coronary Plaque T Cells Are Clonal and Cross-React to Virus and Self.

BACKGROUND: Coronary artery disease is an incurable, life-threatening disease that was once considered primarily a disorder of lipid deposition. Coronary artery disease is now also characterized by chronic inflammation' notable for the buildup of atherosclerotic plaques containing immune cells in various states of activation and differentiation. Understanding how these immune cells contribute to disease progression may lead to the development of novel therapeutic strategies. METHODS: We used single-cell technology and in vitro assays to interrogate the immune microenvironment of human coronary atherosclerotic plaque at different stages of maturity. RESULTS: In addition to macrophages, we found a high proportion of αß T cells in the coronary plaques. Most of these T cells lack high expression of CCR7 and L-selectin, indicating that they are primarily antigen-experienced memory cells. Notably, nearly one-third of these cells express the HLA-DRA surface marker, signifying activation through their TCRs (T-cell receptors). Consistent with this, TCR repertoire analysis confirmed the presence of activated αß T cells (CD4

Highlights of Cardiovascular Disease Studies Presented at the 2021 American Heart Association Scientific Sessions.

PURPOSE OF REVIEW: This review highlights major studies across a broad array of topics presented at the virtual 2021 American Heart Association (AHA) Scientific Sessions. RECENT FINDINGS: Assessed studies examine a remotely delivered hypertension and lipid program in 10,000 patients across a diverse healthcare network; a cluster-randomized trial of a village doctor-led intervention for hypertension control; empagliflozin in heart failure with preserved ejection fraction (EMPEROR-Preserved); efficacy and safety of empagliflozin in hospitalized heart failure patients (EMPULSE); icosapent ethyl versus placebo in outpatients with coronavirus disease 2019 (PREPARE-IT 2); clinical safety, pharmacokinetics, and low-density lipoprotein cholesterol-lowering efficacy of MK-0161, an oral proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor; and effects of aspirin on dementia and cognitive impairment in the ASCEND trial. Research presented at the 2021 AHA Scientific Sessions emphasized the importance of interventions for cardiovascular disease prevention.

Anti-Inflammatory Effects of Curcumin in the Inflammatory Diseases: Status, Limitations and Countermeasures.

Curcumin is a natural compound with great potential for disease treatment. A large number of studies have proved that curcumin has a variety of biological activities, among which anti-inflammatory effect is a significant feature of it. Inflammation is a complex and pervasive physiological and pathological process. The physiological and pathological mechanisms of inflammatory bowel disease, psoriasis, atherosclerosis, COVID-19 and other research focus diseases are not clear yet, and they are considered to be related to inflammation. The anti-inflammatory effect of curcumin can effectively improve the symptoms of these diseases and is expected to be a candidate drug for the treatment of related diseases. This paper mainly reviews the anti-inflammatory effect of curcumin, the inflammatory pathological mechanism of related diseases, the regulatory effect of curcumin on these, and the latest research results on the improvement of curcumin pharmacokinetics. It is beneficial to the further study of curcumin and provides new ideas and insights for the development of curcumin anti-inflammatory preparations.

Large mural thrombus in the non-aneurysmal and non-atherosclerotic ascending aorta: a case report.

BACKGROUND: The mural thrombus in the ascending aorta is rare, most of which are associated with aneurysm or atherosclerotic lesions, with high risks of causing catastrophic thrombotic events. A mural thrombus in the non-aneurysmal and non-atherosclerotic ascending aorta is exceptionally uncommon. CASE PRESENTATION: We reported a large mural thrombus in normal ascending aorta of an asymptomatic patient. Preoperative imaging confirmed the presence of the sessile thrombus located at the left anterior wall of ascending aorta. Given that it had the potential to cause fatal thrombotic complications, surgical removal and segment of ascending aorta replacement were executed. The patient had an uneventful recovery and discharged 14 days after surgery. CONCLUSIONS: Anticoagulant is the therapeutic cornerstone of ascending aortic thrombus, but surgery should be performed aggressively when the thrombus is large or floating to avoid severe embolic complications or recurrence.

Chronic Stress, Exercise and Cardiovascular Disease: Placing the Benefits and Risks of Physical Activity into Perspective.

Chronic stress, which has been exacerbated worldwide by the lingering COVID pandemic, has been strongly linked to cardiovascular disease (CVD). In addition, autonomic dysregulation via sustained sympathetic activity has been shown to increase the risk of arrhythmias, platelet aggregation, acute coronary syndromes and heart failure. Fortunately, effective coping strategies have been shown to attenuate the magnitude of hyperarousal associated with the stress response, including moderate-to-vigorous lifestyle activity and/or structured exercise. A good-to-excellent level of cardiorespiratory fitness also appears to be highly cardioprotective. These beneficial effects have been substantiated by numerous studies that have evaluated the levels of stress reactivity and stress recovery in physically active individuals versus matched sedentary controls, as well as before and after exercise interventions. On the other hand, unaccustomed strenuous exercise in habitually sedentary persons with underlying CVD is associated with a disproportionate incidence of acute cardiac events. Moreover, extreme exercise regimens appear to increase coronary calcification and the likelihood of developing atrial fibrillation. This review summarizes these relations and more, with specific reference to placing the benefits and risks of physical activity into perspective.