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1.
Cells ; 11(7)2022 03 28.
Article in English | MEDLINE | ID: covidwho-1785536

ABSTRACT

The use of cannabis preparations has steadily increased. Although cannabis was traditionally assumed to only have mild vegetative side effects, it has become evident in recent years that severe cardiovascular complications can occur. Cannabis use has recently even been added to the risk factors for myocardial infarction. This review is dedicated to pathogenetic factors contributing to cannabis-related myocardial infarction. Tachycardia is highly important in this respect, and we provide evidence that activation of CB1 receptors in brain regions important for cardiovascular regulation and of presynaptic CB1 receptors on sympathetic and/or parasympathetic nerve fibers are involved. The prototypical factors for myocardial infarction, i.e., thrombus formation and coronary constriction, have also been considered, but there is little evidence that they play a decisive role. On the other hand, an increase in the formation of carboxyhemoglobin, impaired mitochondrial respiration, cardiotoxic reactions and tachyarrhythmias associated with the increased sympathetic tone are factors possibly intensifying myocardial infarction. A particularly important factor is that cannabis use is frequently accompanied by tobacco smoking. In conclusion, additional research is warranted to decipher the mechanisms involved, since cannabis use is being legalized increasingly and Δ9-tetrahydrocannabinol and its synthetic analogue nabilone are indicated for the treatment of various disease states.


Subject(s)
Cannabinoids , Cannabis , Myocardial Infarction , Adolescent , Analgesics , Cannabinoid Receptor Agonists , Cannabinoids/adverse effects , Cannabis/adverse effects , Heart , Humans , Myocardial Infarction/chemically induced , Myocardial Infarction/drug therapy
2.
J Pharmacol Exp Ther ; 381(3): 197-203, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1765068

ABSTRACT

Cardiac rehabilitation (CR) following acute myocardial infarction (AMI) improves physical capacities and decreases hospitalizations and cardiovascular mortality. L-arginine is the substrate used by nitric oxide (NO) synthase to generate NO and it has been shown to exert its beneficial effects on endothelium driving vasodilatation, reducing inflammation, and ameliorating physical function. We hypothesized that L-arginine could enhance physical capacities in patients who underwent CR after AMI. We designed a study aimed to assess the effects of L-arginine administration on the physical capacity of patients who underwent coronary revascularization after AMI. The trial was carried out amid the COVID-19 pandemic. Patients were assigned, with a 2:1 ratio, to add to their standard therapy one bottle containing 1.66 g of L-arginine or one bottle of identical aspect apart from not containing L-arginine, twice a day orally for 3 weeks. Patients performed a 6-minute walking test (6MWT), and their Borg modified 0-10 rating of perceived exertion (BRPE) was assessed before starting and at the end of the treatment. Seventy-five patients receiving L-arginine, and 35 receiving placebo successfully completed the study. The 6MWT distance increased significantly in the L-arginine group compared with both baseline and placebo (P < 0.0001). Additionally, we observed a significant improvement in the BRPE in patients treated with L-arginine but not in the placebo group. Taken together, our data indicate that L-arginine potentiates the response to CR independently of age, sex, baseline functional capacity, and comorbid conditions. SIGNIFICANCE STATEMENT: This study shows for the first time that oral supplementation of L-arginine potentiates the response to cardiac rehabilitation after myocardial infarction and cardiac revascularization. Indeed, we observed a significant improvement in two fundamental parameters, namely, the 6-minute walking test and the Borg modified 0-10 rating of perceived exertion. Strikingly, the beneficial effects of L-arginine were independent of age, sex, comorbid conditions, and baseline functional capacity.


Subject(s)
COVID-19 , Cardiac Rehabilitation , Myocardial Infarction , Arginine , Heart , Humans , Myocardial Infarction/drug therapy , Nitric Oxide Synthase , Pandemics
3.
Am Heart J ; 247: 33-41, 2022 05.
Article in English | MEDLINE | ID: covidwho-1652480

ABSTRACT

BACKGROUND: Activation of inflammatory pathways during acute myocardial infarction contributes to infarct size and left ventricular (LV) remodeling. The present prospective randomized clinical trial was designed to test the efficacy and safety of broad-spectrum anti-inflammatory therapy with a mammalian target of rapamycin (mTOR) inhibitor to reduce infarct size. DESIGN: Controlled-Level EVERolimus in Acute Coronary Syndrome (CLEVER-ACS, clinicaltrials.gov NCT01529554) is a phase II randomized, double-blind, multi-center, placebo-controlled trial on the effects of a 5-day course of oral everolimus on infarct size, LV remodeling, and inflammation in patients with acute ST-elevation myocardial infarction (STEMI). Within 5 days of successful primary percutaneous coronary intervention (pPCI), patients are randomly assigned to everolimus (first 3 days: 7.5 mg every day; days 4 and 5: 5.0 mg every day) or placebo, respectively. The primary efficacy outcome is the change from baseline (defined as 12 hours to 5 days after pPCI) to 30-day follow-up in myocardial infarct size as measured by cardiac magnetic resonance imaging (CMRI). Secondary endpoints comprise corresponding changes in cardiac and inflammatory biomarkers as well as microvascular obstruction and LV volumes assessed by CMRI. Clinical events, laboratory parameters, and blood cell counts are reported as safety endpoints at 30 days. CONCLUSION: The CLEVER-ACS trial tests the hypothesis whether mTOR inhibition using everolimus at the time of an acute STEMI affects LV infarct size following successful pPCI.


Subject(s)
Acute Coronary Syndrome , Anterior Wall Myocardial Infarction , Myocardial Infarction , Percutaneous Coronary Intervention , ST Elevation Myocardial Infarction , Acute Coronary Syndrome/drug therapy , Arrhythmias, Cardiac , Double-Blind Method , Everolimus/therapeutic use , Humans , Magnetic Resonance Imaging , Myocardial Infarction/drug therapy , Prospective Studies , ST Elevation Myocardial Infarction/drug therapy , TOR Serine-Threonine Kinases/therapeutic use , Treatment Outcome , Ventricular Remodeling
4.
Catheter Cardiovasc Interv ; 99(3): 641-649, 2022 02.
Article in English | MEDLINE | ID: covidwho-1513777

ABSTRACT

Plaque rupture leads to a cascade of events culminating in collagen disruption, tissue factor release, platelet activation and thrombus formation. Pro-inflammatory conditions, hyperglycemia and smoking predispose to high thrombus burden (HTB) which is an independent predictor of slow or no-reflow. In patients with acute myocardial infarction (AMI), glycoprotein IIb/IIIa inhibitors (GPI) reduce thrombus burden and improve myocardial perfusion. These agents are typically administered systemically via the intravenous route or locally via an intracoronary (IC) route. However, as higher local concentrations of GPI are associated with enhanced platelet inhibition, intralesional (IL) GPI administration may be particularly effective in cases of HTB. Modest-sized randomized trials comparing IL and IC GPI delivery have reported conflicting outcomes. Some trials have demonstrated improved coronary flow and myocardial perfusion with reduced major adverse cardiac events with IL compared with IC GPI administration, whereas others have shown no significant benefits. Furthermore, although no direct comparison has been made between IL delivery using an aspiration catheter, microcatheter or a dedicated balloon-based "weeping" infusion-catheter, improved outcomes have been most consistent following GPI administration at the site of the lesion and thrombus with the dedicated infusion catheter. This review provides an update on the role and outcomes of IL GPI administration in patients with AMI and HTB. Based on the evidence we offer an algorithm demonstrating when to consider IL administration in patients with AMI undergoing intervention. We conclude with a perspective on the management of patients with STEMI and COVID-19 in whom a prothrombotic state often results in HTB.


Subject(s)
COVID-19 , Myocardial Infarction , Percutaneous Coronary Intervention , Humans , Myocardial Infarction/drug therapy , Percutaneous Coronary Intervention/adverse effects , Percutaneous Coronary Intervention/methods , Platelet Aggregation Inhibitors/adverse effects , Platelet Glycoprotein GPIIb-IIIa Complex , SARS-CoV-2 , Treatment Outcome
5.
Molecules ; 26(21)2021 Oct 31.
Article in English | MEDLINE | ID: covidwho-1512509

ABSTRACT

Atherosclerosis, myocardial infarction (MI) and heart failure (HF) are the main causes of mortality and morbidity around the globe. New therapies are needed to better manage ischemic heart disease and HF as existing strategies are not curative. Resveratrol is a stilbene polyphenolic compound with favorable biological effects that counter chronic diseases. Current evidence suggests that resveratrol is cardioprotective in animal models of atherosclerosis, ischemic heart disease, and HF. Though clinical studies for resveratrol have been promising, evidence remains inadequate to introduce it to the clinical setting. In this narrative review, we have comprehensively discussed the relevant compelling evidence regarding the efficacy of resveratrol as a new therapeutic agent for the management of atherosclerosis, MI and HF.


Subject(s)
Atherosclerosis/drug therapy , Cardiovascular Diseases/drug therapy , Heart Failure/drug therapy , Myocardial Infarction/drug therapy , Resveratrol/therapeutic use , Animals , Humans
6.
N Engl J Med ; 385(20): 1845-1855, 2021 11 11.
Article in English | MEDLINE | ID: covidwho-1510679

ABSTRACT

BACKGROUND: In patients with symptomatic heart failure, sacubitril-valsartan has been found to reduce the risk of hospitalization and death from cardiovascular causes more effectively than an angiotensin-converting-enzyme inhibitor. Trials comparing the effects of these drugs in patients with acute myocardial infarction have been lacking. METHODS: We randomly assigned patients with myocardial infarction complicated by a reduced left ventricular ejection fraction, pulmonary congestion, or both to receive either sacubitril-valsartan (97 mg of sacubitril and 103 mg of valsartan twice daily) or ramipril (5 mg twice daily) in addition to recommended therapy. The primary outcome was death from cardiovascular causes or incident heart failure (outpatient symptomatic heart failure or heart failure leading to hospitalization), whichever occurred first. RESULTS: A total of 5661 patients underwent randomization; 2830 were assigned to receive sacubitril-valsartan and 2831 to receive ramipril. Over a median of 22 months, a primary-outcome event occurred in 338 patients (11.9%) in the sacubitril-valsartan group and in 373 patients (13.2%) in the ramipril group (hazard ratio, 0.90; 95% confidence interval [CI], 0.78 to 1.04; P = 0.17). Death from cardiovascular causes or hospitalization for heart failure occurred in 308 patients (10.9%) in the sacubitril-valsartan group and in 335 patients (11.8%) in the ramipril group (hazard ratio, 0.91; 95% CI, 0.78 to 1.07); death from cardiovascular causes in 168 (5.9%) and 191 (6.7%), respectively (hazard ratio, 0.87; 95% CI, 0.71 to 1.08); and death from any cause in 213 (7.5%) and 242 (8.5%), respectively (hazard ratio, 0.88; 95% CI, 0.73 to 1.05). Treatment was discontinued because of an adverse event in 357 patients (12.6%) in the sacubitril-valsartan group and 379 patients (13.4%) in the ramipril group. CONCLUSIONS: Sacubitril-valsartan was not associated with a significantly lower incidence of death from cardiovascular causes or incident heart failure than ramipril among patients with acute myocardial infarction. (Funded by Novartis; PARADISE-MI ClinicalTrials.gov number, NCT02924727.).


Subject(s)
Aminobutyrates/therapeutic use , Angiotensin Receptor Antagonists/therapeutic use , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Biphenyl Compounds/therapeutic use , Heart Failure/prevention & control , Myocardial Infarction/drug therapy , Ramipril/therapeutic use , Valsartan/therapeutic use , Aged , Aminobutyrates/adverse effects , Angiotensin Receptor Antagonists/adverse effects , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Biphenyl Compounds/adverse effects , Cardiovascular Diseases/mortality , Double-Blind Method , Drug Combinations , Female , Hospitalization/statistics & numerical data , Humans , Hypotension/chemically induced , Male , Middle Aged , Myocardial Infarction/complications , Myocardial Infarction/mortality , Proportional Hazards Models , Ramipril/adverse effects , Stroke Volume , Valsartan/adverse effects , Ventricular Dysfunction, Left/etiology
8.
Herzschrittmacherther Elektrophysiol ; 32(3): 365-370, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1315331

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with cardiovascular (CV) complications including myocardial injury, myocarditis, arrhythmias, and venous thromboembolism. The infection is more severe in patients with pre-existing cardiovascular disease (CVD), where systemic inflammation due to cytokine storm, hypercoagulation, as well as high hematocrit and platelet (PLT) count may contribute to an increased CV risk. The authors hypothesize that anticoagulants and antiplatelets prevent miocardial infarction (MI) in patients with pre-existing CVD. METHODS: A cohort study enrolled patients with a confirmed diagnosis of COVID-19. Clinical and laboratory data, total and CV mortality, as well as MI incidence and treatment regimens were compared according to the time of hospitalization: 40-day period in April-May (Group 1) and in October-November (Group 2). RESULTS: A total of 195 patients were enrolled: 93 in Group 1, with 36.5%, and 102 in Group 2 with 38.2% pre-existing CVD. Group 1 was managed with infusion therapy; only 10.7% received anticoagulation. Group 2 received preventive anticoagulants, antiplatelets, and infusion therapy. In Group 1, seven cases of MI were recorded compared to only three in Group 2. No significant difference in overall mortality (4.3% vs 6.86%, p = 0.441) and MI incidence (7.5% vs 2.9%, p = 0.149) was found, but significant differences were seen in the incidence of severe and critically ill cases between the groups (69.9% and 7.5% vs 75.5% and 20.6%, p < 0.001). CONCLUSIONS: Poorer outcomes in the early COVID-19 wave were associated with inadequate anticoagulation due to lack of knowledge about the new virus. Despite significantly more severe cases, there was no significant difference in overall mortality and MI incidence in patients with anticoagulation.


Subject(s)
COVID-19 , Myocardial Infarction , Anticoagulants/therapeutic use , Cohort Studies , Humans , Myocardial Infarction/drug therapy , Myocardial Infarction/prevention & control , SARS-CoV-2
9.
Platelets ; 32(8): 1009-1017, 2021 Nov 17.
Article in English | MEDLINE | ID: covidwho-1258665

ABSTRACT

Platelets may be a target of bacteria and viruses, which can directly or indirectly activate them so promoting thrombosis. In accordance with this, community-acquired pneumonia (CAP) is complicated by ischemia-related vascular disease (myocardial infarction and stroke) in roughly 10% of patients while the incidence of venous thrombosis is uncertain. In CAP platelet biosynthesis of TxA2 is augmented and associated with myocardial infarction; however, a cause-effect relationship is still unclear as unclear is if platelet activation promotes thrombosis or functional changes of coronary tree such vasospasm. Retrospective studies suggested a potential role of aspirin in reducing mortality but the impact on vascular disease is still unknown. Coronavirus disease 2019 (Covid-19) is complicated by thrombosis in roughly 20% of patients with an almost equivalent localization in arterial and venous circulation. Platelet activation seems to have a pivot role in the thrombotic process in Covid-19 as consistently evidenced by its involvement in promoting Tissue Factor up-regulation via leucocyte interaction. Until now, antiplatelet treatment has been scarcely considered for the treatment of Covid-19; interventional trials, however, are in progress to explore this issue. The aim of this review is 1) to compare the type of vascular diseases complicating CAP and Covid-19 2) to assess the different role of platelets in both diseases and 3) to discuss if antiplatelet treatment is potentially useful to improve clinical outcomes.


Subject(s)
Aspirin/therapeutic use , Blood Platelets/metabolism , COVID-19 , Myocardial Infarction , SARS-CoV-2/metabolism , Stroke , Thrombosis , COVID-19/drug therapy , COVID-19/metabolism , COVID-19/mortality , Humans , Myocardial Infarction/drug therapy , Myocardial Infarction/metabolism , Myocardial Infarction/mortality , Stroke/drug therapy , Stroke/metabolism , Stroke/mortality , Thrombosis/drug therapy , Thrombosis/metabolism , Thrombosis/mortality
10.
BMJ Open ; 10(12): e042390, 2020 12 21.
Article in English | MEDLINE | ID: covidwho-1214972

ABSTRACT

INTRODUCTION: A December 2019 WHO rapid communication recommended the use of 9-month all-oral regimens for treating multidrug-resistant tuberculosis (MDR-TB). Besides the clinical benefits, they are thought to be less costly than the injectable-containing regimens, for both the patient and the health system. STREAM is the first randomised controlled trial with an economical evaluation to compare all-oral and injectable-containing 9-11-month MDR-TB treatment regimens. METHODS AND ANALYSIS: Health system costs of delivering a 9-month injectable-containing regimen and a 9-month all-oral bedaquiline-containing regimen will be collected in Ethiopia, India, Moldova and Uganda, using 'bottom-up' and 'top-down' costing approaches. Patient costs will be collected using questionnaires that have been developed based on the STOP-TB questionnaire. The primary objective of the study is to estimate the cost utility of the two regimens, from a health system perspective. Secondary objectives include estimating the cost utility from a societal perspective as well as evaluating the cost-effectiveness of the regimens, using both health system and societal perspectives. The effect measure for the cost-utility analysis will be the quality-adjusted life years (QALY), while the effect measure for the cost-effectiveness analysis will be the efficacy outcome from the clinical trial. ETHICS AND DISSEMINATION: The study has been evaluated and approved by the Ethics Advisory Group of the International Union Against Tuberculosis and Lung Disease and also approved by ethics committees in all participating countries. All participants have provided written informed consent. The results of the economic evaluation will be published in a peer-reviewed journal. TRIAL REGISTRATION NUMBER: ISRCTN18148631.


Subject(s)
Myocardial Infarction , Antitubercular Agents/therapeutic use , Cost-Benefit Analysis , Diarylquinolines , Ethiopia , Humans , India , Moldova , Myocardial Infarction/drug therapy , Rifampin , Tuberculosis, Multidrug-Resistant/drug therapy , Uganda
12.
J Cell Mol Med ; 25(3): 1342-1349, 2021 02.
Article in English | MEDLINE | ID: covidwho-1030565

ABSTRACT

SARS-CoV-2, the virus responsible for the global coronavirus disease (COVID-19) pandemic, attacks multiple organs of the human body by binding to angiotensin-converting enzyme 2 (ACE2) to enter cells. More than 20 million people have already been infected by the virus. ACE2 is not only a functional receptor of COVID-19 but also an important endogenous antagonist of the renin-angiotensin system (RAS). A large number of studies have shown that ACE2 can reverse myocardial injury in various cardiovascular diseases (CVDs) as well as is exert anti-inflammatory, antioxidant, anti-apoptotic and anticardiomyocyte fibrosis effects by regulating transforming growth factor beta, mitogen-activated protein kinases, calcium ions in cells and other major pathways. The ACE2/angiotensin-(1-7)/Mas receptor axis plays a decisive role in the cardiovascular system to combat the negative effects of the ACE/angiotensin II/angiotensin II type 1 receptor axis. However, the underlying mechanism of ACE2 in cardiac protection remains unclear. Some approaches for enhancing ACE2 expression in CVDs have been suggested, which may provide targets for the development of novel clinical therapies. In this review, we aimed to identify and summarize the role of ACE2 in CVDs.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/complications , Cardiovascular Diseases/metabolism , Angiotensin-Converting Enzyme 2/pharmacology , Animals , Arrhythmias, Cardiac/metabolism , Arrhythmias, Cardiac/physiopathology , COVID-19/drug therapy , COVID-19/metabolism , Cardiovascular Diseases/complications , Cardiovascular Diseases/physiopathology , Diminazene/pharmacology , Heart Failure/etiology , Humans , Hypertension/metabolism , Hypertension/physiopathology , Myocardial Infarction/drug therapy , Myocardial Infarction/metabolism , Myocardial Infarction/physiopathology , Recombinant Proteins/pharmacology
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