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Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (29 November 2024) | Viewed by 15592

Special Issue Editor

Dr. Mohammad Alkhalil

E-Mail Website
Guest Editor
1. Peter Munk Cardiac Centre, Division of Cardiology, Toronto General Hospital, University Health Network, Toronto, ON, Canada
2. Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne, UK
3. Translational and Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK
Interests: atherosclerosis; myocardial Infarction; interventional cardiology; magnetic resonance Imaging

Special Issue Information

Dear Colleagues,

Over the last three decades, significant improvement has been achieved in reducing cardiovascular morbidity and mortality. Nonetheless, one in five patients returns with a second event within 5 years despite being on guidelines of recommended optimal medical therapy. This residual risk is heterogeneous, but characterising the atherosclerosis process allowed tailored therapy and precise intervention at an individual level to reduce cardiovascular residual risk. Recent advances in pharmacotherapy have enabled physicians to target the main atherosclerotic-related risks, namely lipid, thrombosis, and inflammation and subsequent heart failure

This Special Issue will discuss recent advances in cardiovascular drugs and their impact on future outcomes in patients presenting with acute coronary syndrome. You are cordially invited to submit an Original Article or Review Article focusing on related topics to contribute to the next Special Issue entitled “Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside”.

Dr. Mohammad Alkhalil
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiovascular disease
  • coronary heart disease (CHD)
  • acute coronary syndrome (ACS)
  • acute myocardial infarction
  • unstable angina
  • drugs
  • antiplatelet therapy
  • lipid-lowering therapy
  • antithrombotic therapy
  • percutaneous coronary intervention (PCI)
  • side effects
  • bleeding risk

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

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Editorial

Jump to: Research, Review

6 pages, 244 KiB  
Editorial
Advances in Cardiovascular Pharmacology in Atherosclerotic-Related Therapeutic Areas: Addressing Patients’ Clinical Needs
by Muntaser Omari and Mohammad Alkhalil
J. Clin. Med. 2023, 12(11), 3665; https://doi.org/10.3390/jcm12113665 - 25 May 2023
Viewed by 1700
Abstract
Over the last three decades, a significant improvement has been achieved in reducing cardiovascular morbidity and mortality [...] Full article
(This article belongs to the Special Issue Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside)

Research

Jump to: Editorial, Review

12 pages, 278 KiB  
Article
Short-Term Atorvastatin Therapy in Healthy Individuals Results in Unaltered Plasma MMP Levels and Disrupted MMP-7 Correlation with Blood Lipids and Blood Count-Derived Inflammatory Markers
by Ion Bogdan Mănescu, Măriuca Mănescu, Laura Iulia Bărcuțean, Liliana Demian and Minodora Dobreanu
J. Clin. Med. 2024, 13(16), 4743; https://doi.org/10.3390/jcm13164743 - 13 Aug 2024
Cited by 1 | Viewed by 1491
Abstract
Background: Matrix metalloproteinases (MMPs) play an important role in the pathophysiology of atherosclerosis. Reportedly, statins can decrease MMP activity in patients with atherosclerotic cardiovascular disease, but this effect has not been studied in healthy individuals. Methods: MMPs 2, 7, and 9 [...] Read more.
Background: Matrix metalloproteinases (MMPs) play an important role in the pathophysiology of atherosclerosis. Reportedly, statins can decrease MMP activity in patients with atherosclerotic cardiovascular disease, but this effect has not been studied in healthy individuals. Methods: MMPs 2, 7, and 9 and several other parameters were measured before and after a four-week course of moderate-dose atorvastatin (20 mg/day) in 21 healthy individuals. Results: Atorvastatin treatment resulted in lower total cholesterol, LDL-cholesterol, non-HDL-cholesterol, and triglycerides (p < 0.001 for all), but higher levels of plasma enzymes AST, ALT, CK, and LDH (p < 0.05 for all). No effect of atorvastatin on plasma MMP median concentrations was recorded. Before treatment, moderate positive significant correlations were found between MMP-7 and age, blood lipids, and blood count-derived inflammatory markers. Pre-treatment MMP-7 was best predicted by the total cholesterol-to-HDL cholesterol ratio in a remnant cholesterol-weighted least squares regression model. After atorvastatin treatment, MMP-7 no longer correlated with these markers. Conclusions: While the effect of statins on plasma MMPs in atherosclerosis is controversial, short-term moderate-dose atorvastatin treatment does not seem to affect levels of MMPs 2, 7, and 9 in healthy individuals. However, an intriguing correlation between MMP-7 and atherosclerosis-related blood lipids and neutrophil-associated inflammatory biomarkers seems to be disrupted by atorvastatin independently of hsCRP, possibly via pleiotropic effects. Full article
(This article belongs to the Special Issue Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside)

Review

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12 pages, 8269 KiB  
Review
Role of Lipoprotein(a) Reduction in Cardiovascular Disease
by Uma Schuth, Kieran Gill, Pyotr Telyuk, Bilal-Reshad Bawamia, David Austin and Azfar Zaman
J. Clin. Med. 2024, 13(21), 6311; https://doi.org/10.3390/jcm13216311 - 22 Oct 2024
Viewed by 2451
Abstract
Recent studies have shown that lipoprotein(a) (Lp(a)) is an important risk factor for a plethora of different cardiovascular diseases. It has been proven that Lp(a) levels are genetically determined and correlate with risk of cardiovascular disease, independent of lifestyle factors. As of yet, [...] Read more.
Recent studies have shown that lipoprotein(a) (Lp(a)) is an important risk factor for a plethora of different cardiovascular diseases. It has been proven that Lp(a) levels are genetically determined and correlate with risk of cardiovascular disease, independent of lifestyle factors. As of yet, treatment options to reduce Lp(a) levels are limited, but new research into Lp(a) reduction yields promising results. This review delves into Lp(a)’s biochemistry and mechanism of effect, the association between Lp(a) and cardiovascular diseases, and possible therapies to minimise cardiovascular disease. Full article
(This article belongs to the Special Issue Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside)
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19 pages, 3442 KiB  
Review
Fractalkine Signalling (CX3CL1/CX3CR1 Axis) as an Emerging Target in Coronary Artery Disease
by Shu Xian Loh, Yasemin Ekinci, Luke Spray, Visvesh Jeyalan, Thomas Olin, Gavin Richardson, David Austin, Mohammad Alkhalil and Ioakim Spyridopoulos
J. Clin. Med. 2023, 12(14), 4821; https://doi.org/10.3390/jcm12144821 - 21 Jul 2023
Cited by 13 | Viewed by 4865
Abstract
Acute myocardial infarction (MI) is the most common and dramatic complication of atherosclerosis, which, despite successful reperfusion therapy, can lead to incident heart failure (HF). HF occurs when the healing process is impaired due to adverse left ventricular remodelling, and can be the [...] Read more.
Acute myocardial infarction (MI) is the most common and dramatic complication of atherosclerosis, which, despite successful reperfusion therapy, can lead to incident heart failure (HF). HF occurs when the healing process is impaired due to adverse left ventricular remodelling, and can be the result of so-called ischaemia/reperfusion injury (IRI), visualised by the development of intramyocardial haemorrhage (IMH) or microvascular obstruction (MVO) in cardiac MRI. Thus far, translation of novel pharmacological strategies from preclinical studies to target either IRI or HF post MI have been largely unsuccessful. Anti-inflammatory therapies also carry the risk of affecting the immune system. Fractalkine (FKN, CX3CL1) is a unique chemokine, present as a transmembrane protein on the endothelium, or following cleavage as a soluble ligand, attracting leukocyte subsets expressing the corresponding receptor CX3CR1. We have shown previously that the fractalkine receptor CX3CR1 is associated with MVO in patients undergoing primary PCI. Moreover, inhibition of CX3CR1 with an allosteric small molecule antagonist (KAND567) in the rat MI model reduces acute infarct size, inflammation, and IMH. Here we review the cellular biology of fractalkine and its receptor, along with ongoing studies that introduce CX3CR1 as a future target in coronary artery disease, specifically in patients with myocardial infarction. Full article
(This article belongs to the Special Issue Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside)
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14 pages, 711 KiB  
Review
The Emerging Role of Icosapent Ethyl in Patients with Cardiovascular Disease: Mechanistic Insights and Future Applications
by Ashish Gupta and Mohammad Alkhalil
J. Clin. Med. 2023, 12(11), 3758; https://doi.org/10.3390/jcm12113758 - 30 May 2023
Cited by 3 | Viewed by 4159
Abstract
Omega-3 polyunsaturated fatty acids (PUFAs) were early established as therapeutic option for patients with high triglyceride levels. Their effects on lipoprotein particles, including a reduction in very low-density lipoprotein and a shift from small to large low-density lipoprotein, is increasingly recognised. This is [...] Read more.
Omega-3 polyunsaturated fatty acids (PUFAs) were early established as therapeutic option for patients with high triglyceride levels. Their effects on lipoprotein particles, including a reduction in very low-density lipoprotein and a shift from small to large low-density lipoprotein, is increasingly recognised. This is coupled with their ability to be incorporated within the cellular membrane, leading to plaque stability and anti-inflammatory effects. Nonetheless, recent clinical trials have not been consistent in demonstrating the potential cardioprotective effects of omega-3 fatty acids. This is despite the circumstantial evidence from imaging studies illustrating the stabilising effects on atherosclerotic plaques and slowing of plaque progression. In this article, we will review the effects of omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on lipid biomarkers, atherosclerotic plaque features, and clinical outcome studies and provide a mechanistic role in managing residual risk of atherosclerosis. This will provide better insight into the inconsistency of the recently reported clinical outcome studies. Full article
(This article belongs to the Special Issue Advances in Drugs and Therapy for Cardiovascular Disease: From the Researcher's Desk to the Patient's Bedside)
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