A better IInflammation is the Mediterranean diet: eat healfh of Inflammation and cardiovascular health, fruits, and nuts, and choose the Performance boosting plugins fats found in avocados, fish and olive oil. Inclisiran in patients at high cardiovascular risk with elevated LDL cholesterol. Medicine ;e Access options Access through your institution. NLRP3 Inflammasome Pathway and Therapeutic Targets.

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Inflammation and Heart Health

Inflammation and cardiovascular health -

Monocytes and macrophages are the major cell types dominating the inflammatory process [ 2 ]. In an acute injury, as observed in myocardial infarction, the temporal dynamics of monocytes are controlled by cytokines and chemokines produced during this process, which in turn give rise to inflammatory and reparative macrophages [ 3 ].

Inflammatory macrophages amplify cytokine signals [IL-1β, IL-6, IL, nitric oxide] and release chemokines to recruit more inflammatory cells. In addition, they are involved with phagocytosis of cellular debris. Following, the clean-up phase, reparative macrophages promote deposition of new extracellular matrix, cell growth and regeneration.

Macrophages also display anti-inflammatory profile, by serving as mediators in the resolution of the inflammatory process, as noted by the high production of IL, TGFβ, and IGF-1 [ 4 ], which assists in the progression from the inflammatory to the regenerative phase of repair.

Inflammatory macrophages must be tightly regulated since the inflammatory cytokines and ROS species released can directly cause myofiber lysis, exacerbating the injury. The pivotal role of innate immunity, especially macrophages, is shown in a recent study showing that a clonal population of granulocytes carrying driver mutation related to haematopoiesis can cause tissue inflammation leading to atherosclerotic diseases [ 5 ].

The role of the adaptive immune system has shown an association with CVD risk due to a sustained and chronic inflammatory state.

T and B cells in the atherosclerotic plaque have been hypothesized to generate an autoimmune-mediated process leading to vascular inflammation [ 6 ]. Another interesting aspect is that inflammation and CVD risk are not limited to disease processes.

Chronic inflammatory processes, as seen in periodontitis [ 7 ], irritable bowel syndrome [ 8 ], and rheumatoid arthritis [ 9 ] can potentially increase the risk of CVDs. Recent evidence suggests that arrhythmogenic diseases including atrial fibrillation, arrhythmogenic cardiomyopathy, cardiac sarcoidosis, and QT prolongation, can have an inflammatory component.

The role of innate and adaptive cells and associated molecular pathways involved in the development and outcome of CVD opens new unconventional treatment options. Consequently, considering the inflammatory involvement in CVDs, many clinical approaches have targeted both aspects of the innate and adaptive immune systems with inflammation-inhibiting agents.

Several clinical studies, including the CANTOS, CIRT and COLCOT trials, provided evidence that modulation of the inflammatory response can potentially reduce the risk for major CV events.

The CANTOS Canakinumab Anti-inflammatory Thrombosis Outcomes Study study suggests that reducing inflammation via antibody IL-1β targeting, without lowering the lipid levels can significantly reduce cardiovascular event rates [ 11 ]. In contrast, low-dose methotrexate did not show a reduction in plasma markers of inflammation in the Cardiovascular Inflammation Reduction Trial CIRT.

Nevertheless, new evidence supports the role of inflammation in atherosclerosis development as seen in the Colchicine Cardiovascular Outcomes Trial COLCOT [ 12 ]. The study showed that colchicine could significantly reduce the CV events in patients after myocardial infarction [ 13 ]. The underlying mechanism behind the reduction of CV events is likely to include direct inhibition of the NLRP3 inflammasome, TNF-α, IL, and IL-6, in addition to IL-1β [ 14 ].

Based on the clinical and experimental data, future therapies might be directed toward a combination of lipid-lowering and inflammation-inhibiting agents in patients with CVDs [ 15 ]. However, the risks and implications of inhibiting inflammation in the treatment of CVD in the host response to infection is yet another aspect to be studied.

Understanding cell-mediated immunology and molecular pathways behind CVDs is paramount in the development and implementation of effective anti-inflammatory and immune-modulating therapies for patients with CVD.

Currently, we have state-of-the-art techniques at our disposal, including advanced in vivo imaging, genome-wide association studies, transgenic lineage tracing mice, mendelian randomization studies, and clinical trials to acquire a deep understanding of the immune landscape involving CVDs.

In summary, we expect this article collection to gather evidences in both basic and clinical research in the CVD field to reinforce existing knowledge and open new therapeutic opportunities for treating these disorders. Frangogiannis NG, Smith CW, Entman ML. The inflammatory response in myocardial infarction.

Cardiovasc Res. Arnold L, Henry A, Poron F, Baba-Amer Y, van Rooijen N, Plonquet A, Gherardi RK, Chazaud B. Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis.

J Exp Med. Tonkin J, Temmerman L, Sampson RD, Gallego-Colon E, Barberi L, Bilbao D, Schneider MD, Musarò A, Rosenthal N. Mol Ther. Frangogiannis NG. The inflammatory response in myocardial injury, repair, and remodelling.

Nat Rev Cardiol. Jaiswal S, Ebert BL. Clonal hematopoiesis in human aging and disease. Wolf D, Ley K. Immunity and Inflammation in Atherosclerosis. Circ Res. Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M.

Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis. J Gen Intern Med. Bigeh A, Sanchez A, Maestas C, Gulati M.

Inflammatory bowel disease and the risk for cardiovascular disease: does all inflammation lead to heart disease? Trends Cardiovasc Med. Skeoch S, Bruce IN.

Atherosclerosis in rheumatoid arthritis: is it all about inflammation? Nat Rev Rheumatol. Lazzerini PE, Capecchi PL, El-Sherif N, Laghi-Pasini F, Boutjdir M. Emerging Arrhythmic Risk of Autoimmune and Inflammatory Cardiac Channelopathies.

J Am Heart Assoc. Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, et al. Antiinflammatory therapy with Canakinumab for atherosclerotic disease. N Engl J Med. Article CAS PubMed Google Scholar.

Tardif J-C, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, et al. Efficacy and safety of low-dose colchicine after myocardial infarction. A study that analyzed Medicare data from more than 1. Shared heart disease risk factors such as high cholesterol and diabetes , along with inactivity and the use of nonsteroidal anti-inflammatory drugs NSAIDs also increase the risk.

The best advice is to work with your rheumatologist to get arthritis under control and ensure you have the lowest amount of systemic inflammation possible. For many people, this includes taking medications. The problem is that while arthritis drugs can help ease joint symptoms, some are also hard on the heart.

At least one arthritis drug may be heart protective. Colchicine is an inexpensive and generally safe anti-inflammatory used for years to treat gout. But your risk goes up with obesity, high blood pressure, diabetes, high cholesterol and smoking.

And you can take measures to lower the risk through some lifestyle changes. The best place to start? A dose of daily exercise and an anti-inflammatory eating plan like the Mediterranean diet. Many studies have shown that people who exercise are less likely to have a heart attack or other serious heart problem.

Hundreds of studies have also shown that exercise can significantly reduce inflammation, relieve arthritis pain and improve mobility. The American Heart Association recommends 30 minutes of aerobic exercise most days and resistance or weight training a few times a week. Swimming is a good option because the water helps support your joints, but a pool might not be accessible.

The same consistency in following a healthy eating plan is also key. Get involved with the arthritis community. Arthritis and Heart Disease Learn how having arthritis can affect heart health and what you can do to protect yourself. Medications and Heart Risk The best advice is to work with your rheumatologist to get arthritis under control and ensure you have the lowest amount of systemic inflammation possible.

Tofacitinib Xeljanz increases the risk of heart attack, stroke, serious blood clots and death. It along with two other JAK inhibitor drugs — baricitinib Olumiant and upadacitinib Rinvoq — carry the strongest warning from the Food and Drug Administration FDA.

If you take one of these drugs, talk to your doctor about switching or ask for a different medication to start with, especially if you have heart disease risk factors.

Disease-modifying antirheumatic drugs DMARDs. Methotrexate and other conventional synthetic DMARDs are the most commonly prescribed medicines for RA, PsA and some other forms of inflammatory arthritis. An analysis of 14 trials based on claims and national databases such as Medicare, Medicaid and the VA found that these drugs carry a greater risk of heart attack and stroke compared to tumor necrosis factor TNF blocker biologics, like adalimumab Humira and etanercept Enbrel.

Researchers suspect this may be because patients taking TNF blockers have better controlled inflammation and use fewer corticosteroids and nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs NSAIDs also increase the risk of heart attack and stroke. In , the FDA cautioned they can lead to life -threatening heart events within just a few weeks of use. The risk increases with longer use and higher doses.

New research shows little heatlh of infection from prostate biopsies. Discrimination at work Inflammation and cardiovascular health cardioovascular to high blood pressure. Icy fingers cardiovaecular toes: Poor circulation or Raynaud's phenomenon? My doctor says I'm at risk for a heart attack because a test shows inflammation. I know about high cholesterol and blood pressure, but how does inflammation increase the risk for heart attacks? I can understand why you're puzzled.