Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 11 de 11
Filter
1.
Braz J Biol ; 82: e267633, 2023.
Article in English | MEDLINE | ID: covidwho-2197513

ABSTRACT

Carnitine is a conditionally necessary vitamin that aids in energy creation and fatty acid metabolism. Its bioavailability is higher in vegetarians than in meat-eaters. Deficits in carnitine transporters occur because of genetic mutations or in conjunction with other illnesses. Carnitine shortage can arise in health issues and diseases-including hypoglycaemia, heart disease, starvation, cirrhosis, and ageing-because of abnormalities in carnitine control. The physiologically active form of L-carnitine supports immunological function in diabetic patients. Carnitine has been demonstrated to be effective in the treatment of Alzheimer's disease, several painful neuropathies, and other conditions. It has been used as a dietary supplement for the treatment of heart disease, and it also aids in the treatment of obesity and reduces blood glucose levels. Therefore, L-carnitine shows the potential to eliminate the influences of fatigue in COVID-19, and its consumption is recommended in future clinical trials to estimate its efficacy and safety. This review focused on carnitine and its effect on tissues, covering the biosynthesis, metabolism, bioavailability, biological actions, and its effects on various body systems and COVID-19.


Subject(s)
COVID-19 , Heart Diseases , Humans , Carnitine/pharmacology , Carnitine/therapeutic use , Dietary Supplements , Liver Cirrhosis , Heart Diseases/drug therapy
2.
Clin Appl Thromb Hemost ; 28: 10760296221141449, 2022.
Article in English | MEDLINE | ID: covidwho-2162206

ABSTRACT

OBJECTIVE: Our objective in this study was to determine the predictive factors of thromboembolic complications in patients with previous heart disease and severe covid-19 infection and the impact of previous use of antithrombotics on protection against these complications. METHODS: We conducted a single-center retrospective study of 158 patients with heart disease admitted to an intensive care unit for severe SARS-COV-2 infection. In order to determine the predictive factors, we used logistic regression analysis. RESULTS: Out of 158 patients, 22 were complicated by a thrombo-embolic event (13.9%), mean age of our population 64.03 (SD = 15.27), with a male predominance of 98 (62%). For the predictive factors of thromboembolic complications, and after multivariate analysis, we find the short duration of hospitalization (OR = 0.92; 95%CI (0.863-0.983), P = .014, previous use of antithrombotic drugs ((OR = 0.288, 95%CI (0.091-0.911), P = .034 for antiplatelet agents) and (OR = 0.322, 95% CI (0, 131-0.851), P = .021) for anticoagulants) as protective factors, and admission thrombocytosis as a risk factor (OR = 4.58, 95%CI (1.2-10.627), P = .021). D-dimer was not detected as a risk factor, and this can be explained by the characteristics of our population. Although prior use of antithrombotic drugs protects against thromboembolic complications during severe infection, there was no benefit in mortality. CONCLUSION: Prior use of antithrombotic drugs is a protective factor against thromboembolic complications in patients with a history of heart disease but without effect on mortality.


Subject(s)
COVID-19 , Cardiovascular Diseases , Heart Diseases , Thromboembolism , Humans , Male , Female , Fibrinolytic Agents/therapeutic use , COVID-19/complications , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/complications , Retrospective Studies , SARS-CoV-2 , Thromboembolism/drug therapy , Thromboembolism/etiology , Thromboembolism/prevention & control , Anticoagulants , Heart Diseases/drug therapy
3.
Ther Adv Cardiovasc Dis ; 16: 17539447221137170, 2022.
Article in English | MEDLINE | ID: covidwho-2139019

ABSTRACT

BACKGROUND: Management of high blood pressure (BP) typically requires adherence to medication regimes. However, it is known that the COVID-19 pandemic both interrupted access to some routine prescriptions and changed some patient health behaviours. AIM: This study, therefore, retrospectively investigated prescription reimbursement of cardiovascular (CVD) medicines as a proxy measure for patient adherence and access to medicines during the pandemic. METHODS: A cohort study of all primary care patients in England prescribed CVD medicines. The exposure was to the global pandemic. Prescriptions were compared before and after the pandemic's onset. Statistical variation was the outcome of interest. RESULTS: Descriptive statistics show changes to monthly prescriptions, with wide confidence intervals indicating varying underlying practice. Analysis of variance reveals statistically significant differences for bendroflumethiazide, potassium-sparing diuretics, nicorandil, ezetimibe, ivabradine, ranolazine, colesevelam and midodrine. After the pandemic began (March-October 2020), negative parameters are observed for ACE inhibitors, beta-blockers, calcium channel blockers, statins, antiplatelet, antithrombotics, ARBs, loop diuretics, doxazosin, bendroflumethiazide, nitrates and indapamide, indicating decelerating monthly prescription items (statistically significant declines of calcium channel blockers, antithrombotic, adrenoreceptor blockers and diuretics) of CVD medicines within the general population. Many data points are not statistically significant, but fluctuations remain clinically important for the large population of patients taking these medications. CONCLUSION: A concerning decline in uptake of CVD therapies for chronic heart disease was observed. Accessible screening and treatment alongside financial relief on prescription levies are needed. A video abstract is (4 min 51 s) available: https://bit.ly/39gvEHi.


Subject(s)
COVID-19 , Cardiovascular Agents , Cardiovascular Diseases , Heart Diseases , Humans , Pandemics , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Bendroflumethiazide , Retrospective Studies , Cohort Studies , Angiotensin Receptor Antagonists , Cardiovascular Agents/adverse effects , Cardiovascular Diseases/diagnosis , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/epidemiology , Heart Diseases/drug therapy , Diuretics/therapeutic use , Drug Prescriptions
4.
BMJ Case Rep ; 14(2)2021 Feb 23.
Article in English | MEDLINE | ID: covidwho-1099755

ABSTRACT

We report a case of cardiac injury in a 46-year-old man affected by COVID-19. The patient presented with shortness of breath and fever. ECG revealed sinus tachycardia with ventricular extrasystoles and T-wave inversion in anterior leads. Troponin T and N-terminal pro B-type natriuretic peptide were elevated. Transthoracic echocardiography showed severely reduced systolic function with an estimated left ventricle ejection fraction of 30%. A nasopharingeal swab was positive for SARS-CoV-2. On day 6, 11 days after onset of symptoms, the patient deteriorated clinically with new chest pain and type 1 respiratory failure. Treatment with colchicine 0.5 mg 8-hourly resulted in rapid clinical resolution. This case report highlights how cardiac injury can dominate the clinical picture in COVID-19 infection. The role of colchicine therapy should be further studied to determine its usefulness in reducing myocardial and possibly lung parenchymal inflammatory responses.


Subject(s)
COVID-19 Drug Treatment , COVID-19/complications , Colchicine/therapeutic use , Heart Diseases/drug therapy , Heart Diseases/virology , Chest Pain/virology , Echocardiography , Humans , Male , Middle Aged , Myocardium/pathology , Natriuretic Peptide, Brain/blood , Peptide Fragments/blood , Systole , Troponin T/blood
5.
Discov Med ; 30(161): 155-161, 2020.
Article in English | MEDLINE | ID: covidwho-1085799

ABSTRACT

SARS-CoV-2 is a novel coronavirus responsible for the global coronavirus 2019 pandemic (COVID-19), which started in early 2020 and is still ongoing today. COVID-19 has caused more than 1 million deaths worldwide and about 50 million infected. COVID-19 not only causes lung injury, but there may also be an involvement of other organs, including the cardiovascular system. SARS-CoV-2 penetrates host cells through the angiotensin 2 conversion enzyme (ACE-2). ACE-2 is expressed in the lungs, heart, testicles, liver, gastrointestinal tract, etc. Several studies have found that a sizeable percentage of patients with severe COVID-19 also have cardiac lesions, including myocardial fibrosis, edema, and pericarditis. Pathological remodeling of the extracellular matrix caused by SARS-CoV-2 leads to fibrotic lesions of myocardial tissue. These fibrotic lesions can cause cardiac dysfunction, reducing the ejection fraction caused by the presence of stiffened myocardial matrix and leading to heart failure, or cause an alteration in electrical conductance by creating cardiac arrhythmias. These cardiac dysfunctions can be fatal if left untreated and managed. It is therefore essential to identify cardiac involvement early in order to act with appropriate treatments to preserve the integrity of the heart. In this review, we describe what is known about cardiac damage from COVID-19, including the scientific rationale for effective therapeutic solutions to combat cardiac injury, and reduce or avoid cardiac damage from COVID-19.


Subject(s)
COVID-19/complications , COVID-19/pathology , Heart Diseases/drug therapy , Heart Diseases/etiology , Myocardium/pathology , SARS-CoV-2/physiology , COVID-19/virology , Humans , Models, Biological , Risk Factors
6.
Acta Diabetol ; 58(7): 831-843, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1083870

ABSTRACT

The outbreak of coronavirus disease 2019 (COVID-19) caused by a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a pandemic. The cellular receptor for SARS-CoV-2 entry is the angiotensin-converting enzyme 2, a membrane-bound homolog of angiotensin-converting enzyme. Henceforth, this has brought the attention of the scientific community to study the interaction between COVID-19 and the renin-angiotensin system (RAS), as well as RAS inhibitors. However, these inhibitors are commonly used to treat hypertension, chronic kidney disorder, and diabetes. Obesity is a known risk factor for heart disease, diabetes, and hypertension, whereas diabetes and hypertension may be indirectly related to each other through the effects of obesity. Furthermore, people with hypertension, obesity, diabetes, and other related complications like cardiovascular and kidney diseases have a higher risk of severe COVID-19 infection than the general population and usually exhibit poor prognosis. This severity could be due to systemic inflammation and compromised immune response and RAS associated with these comorbid conditions. Therefore, there is an urgent need to develop evidence-based treatment methods that do not affect the severity of COVID-19 infection and effectively manage these chronic diseases in people with COVID-19.


Subject(s)
COVID-19/mortality , Diabetes Mellitus/epidemiology , Hypertension/epidemiology , Obesity/epidemiology , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Antihypertensive Agents/pharmacology , Antihypertensive Agents/therapeutic use , COVID-19/complications , COVID-19/epidemiology , Comorbidity , Diabetes Complications/drug therapy , Diabetes Complications/epidemiology , Diabetes Complications/mortality , Diabetes Mellitus/drug therapy , Disease Progression , Heart Diseases/complications , Heart Diseases/drug therapy , Heart Diseases/epidemiology , Humans , Hypertension/complications , Hypertension/drug therapy , Obesity/complications , Pandemics , Peptidyl-Dipeptidase A/physiology , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiology , Risk Factors , SARS-CoV-2/drug effects , SARS-CoV-2/physiology
7.
ACS Appl Mater Interfaces ; 13(1): 312-323, 2021 Jan 13.
Article in English | MEDLINE | ID: covidwho-997781

ABSTRACT

In this study, we present a modulated synthesis nanocrystalline defective UiO-66 metal-organic framework as a potential chloroquine diphosphate (CQ) delivery system. Increasing the concentration of hydrochloric acid during the modulated synthesis resulted in a considerable increase of pore volume, which enhanced the CQ loading in CQ@UiO-66 composites. Drug release tests for CQ@UiO-66 composites have confirmed prolonged CQ release in comparison with pure CQ. In vivo tests on a Danio reiro model organism have revealed that CQ released from CQ@UiO-66 25% showed lower toxicity and fewer cardiotoxic effects manifested by cardiac malformations and arrhythmia in comparison to analogous doses of CQ. Cytotoxicity tests proved that the CQ loaded on the defective UiO-66 cargo resulted in increased viability of cardiac cells (H9C2) as compared to incubation with pure CQ. The experimental results presented here may be a step forward in the context of reducing the cardiotoxicity CQ.


Subject(s)
Chloroquine/analogs & derivatives , Heart Diseases/drug therapy , Metal-Organic Frameworks/pharmacology , Nanoparticles/chemistry , Animals , Chloroquine/adverse effects , Chloroquine/chemistry , Chloroquine/pharmacology , Disease Models, Animal , Drug Delivery Systems/adverse effects , Drug Liberation/drug effects , HEK293 Cells , Heart Diseases/chemically induced , Heart Diseases/pathology , Humans , Hydrochloric Acid/pharmacology , Metal-Organic Frameworks/chemistry , Organometallic Compounds/chemistry , Organometallic Compounds/pharmacology , Phthalic Acids/chemistry , Phthalic Acids/pharmacology , Zebrafish/genetics
8.
Cardiovasc Drugs Ther ; 35(3): 427-440, 2021 06.
Article in English | MEDLINE | ID: covidwho-754431

ABSTRACT

Lopinavir-ritonavir combination is being used for the treatment of SARS-CoV-2 infection. A low dose of ritonavir is added to other protease inhibitors to take advantage of potent inhibition of cytochrome (CYP) P450 3A4, thereby significantly increasing the plasma concentration of coadministered lopinavir. Ritonavir also inhibits CYP2D6 and induces CYP2B6, CYP2C19, CYP2C9, and CYP1A2. This potent, time-dependent interference of major hepatic drug-metabolizing enzymes by ritonavir leads to several clinically important drug-drug interactions. A number of patients presenting with acute coronary syndrome and acute heart failure may have SARS-CoV-2 infection simultaneously. Lopinavir-ritonavir is added to their prescription of multiple cardiac medications leading to potential drug-drug interactions. Many cardiology, pulmonology, and intensivist physicians have never been exposed to clinical scenarios requiring co-prescription of cardiac and antiviral therapies. Therefore, it is essential to enumerate these drug-drug interactions, to avoid any serious drug toxicity, to consider alternate and safer drugs, and to ensure better patient care.


Subject(s)
COVID-19 Drug Treatment , Heart Diseases/drug therapy , Lopinavir/administration & dosage , Ritonavir/administration & dosage , SARS-CoV-2 , Anticoagulants/therapeutic use , Drug Interactions , Drug Therapy, Combination , Humans , Hypolipidemic Agents/therapeutic use , Platelet Aggregation Inhibitors/therapeutic use
SELECTION OF CITATIONS
SEARCH DETAIL