What Causes Calcium Deposits In The Heart – Researchers illustrate the power of a low coronary artery calcium (CAC) score in the context of heart disease in a new study published in the Journal of the American College of Cardiology. In light of the new findings, the authors argue for adding the CAC score to factors considered before doctors prescribe drugs such as statins.

Even in the presence of other known risk factors, including diabetes, high blood pressure and bad cholesterol, the researchers found that minimal calcium build-up in the coronary arteries, which supply the heart with blood and oxygen, reduced the risk of “cardiovascular events”. ” up to three percent for at least ten years. The higher the calcium build-up, the higher the risk of heart attack and stroke.

What Causes Calcium Deposits In The Heart

The American Heart Association recommends that people should start statin therapy when they reach a 7.5 percent risk of a cardiovascular event, based on a CAC score obtained by computed tomography, which is simple, affordable, and reflects a person’s 10-year risk.

Causes Of Pulmonary Calcification*

“Our findings suggest that individuals without calcium build-up in their arteries may not need statins regardless of other risk factors for coronary heart disease,” explained Dr. Parag Joshi.

How does calcium initially enter the blood vessels? Atherosclerosis causes plaque to calcify over time. Thus, coronary artery calcium is a marker of atherosclerosis, coronary heart disease, and coronary microvascular disease.

Arterial calcification can be intimal or medial, each associated with different risk factors. Scientists previously thought that coronary artery calcification was a benign, normal consequence of aging. But they quickly realized that it actually causes hardening of the arteries, which affects 90 percent of men and 67 percent of women over the age of 70.

Risk factors for CVD include high BMI, high blood pressure, glucose abnormalities, family history of CVD, and chronic kidney disease. CAC is not affected by dietary calcium intake.

Warfarin Induced Calcification: Potential Prevention And Treatment Strategies

The new study examined CT scan data from the Multi-Ethnic Study of Atherosclerosis (MESA) of more than six thousand people who had never had a heart attack or stroke. Half of the participants had no calcium deposits, resulting in a CAC score of zero. A score of zero does not mean zero risk; the risk is only small and not high enough to require statin therapy.

“The CAC score can really inform the doctor-patient discussion about starting a statin for the primary prevention of heart attacks and strokes,” said Dr. Joshi. Other factors, such as family history, need to be taken into account, the researchers say, because preventive statin treatment can prevent future heart problems.

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Major Study Of Atherosclerotic Plaque Deposits Shows Potential Breakthrough In Determining Risk For Heart Attacks

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By Francesco Vieceli Dalla Sega Francesco Vieceli Dalla Sega Scilit Preprints.org Google Scholar View Publications 1 , Francesca Fortini Francesca Fortini Scilit Preprints.org Google Scholar View Publications 1 , Paolo Severi Paolo Severi Scilit Preprints.org Google Scholar Paola Rizzo Publications 2 Rizzo Scilit Preprints.org Google Scholar View Publications 1, 2 , Iija Gardi Iija Gardi Scilit Preprints.org Google Scholar View Publications 1 , Paolo Cimaglia Paolo Cimaglia Scilit Preprints.org Google Scholar View Publications 1 , Claudio Rapezzi Claudit Preprints Scilit Google Scholar View Publications 1, 2 , Luigi Tavazzi Luigi Tavazzi Scilit Preprints.org Google Scholar View Publications 1 and Roberto Ferrari Roberto Ferrari Scilit Preprints.org Google Scholar View Publications 2, 3, *

Metastatic Pulmonary Calcification And End Stage Renal Disease

Laboratory of Advanced Therapies Technologies (LTTA), Department of Translational Medicine, University of Ferrara, Via Fossato di Mortara 64/B, 44121 Ferrara, Italy

Received: 2022 January 26 / Revised: 2022 February 21 / Adopted: 2022 March 7 / Published: 2022 March 9

Considering the aging of the population and the increased impact of risk factors, the clinical significance of vascular calcification has increased in recent years. Tissue calcification is often the point of no return, leaving no room for any medical therapy and limiting the possibility of surgical and interventional treatment, a real insurmountable obstacle. Due to the proliferation of cardiac imaging techniques, cardiac calcifications of various levels and extents are increasingly recognized. The pathogenesis of calcifications is not unique, but involves different mechanisms depending on the specific site and disease, which in turn lead to different phenotypes. Unfortunately, clinicians are not always aware of these different mechanisms and phenotypes. This concise but thorough review examines the various molecular processes and their associations with specific clinical conditions and current therapeutic approaches to combat calcification.

There is increasing interest in arterial and heart valve calcifications as they contribute to cardiovascular outcomes and are major predictors of cardiovascular and renal disease. Cardiovascular calcifications are often considered a single disease, but they are essentially multifactorial disorders arising in different environments and biological phenotypes, through different pathways. Here, we examine each distinct molecular process, its relative relationship to a specific clinical condition, and current therapeutic approaches to combat calcification. So, first of all, we study the features of calcium deposition in blood vessels and valves, because it occurs in different tissues, responds differently to shear stress, has a specific etiology and time of calcification. We then distinguish the mechanisms and pathways leading to hyperphosphatemic calcification, characteristic of the medial layer of the vessel and mainly associated with chronic kidney disease, from inflammation, characteristic of intimal vascular calcification, which is most common in atherosclerotic vascular diseases. Finally, we study calcifications resulting from rheumatic valvular disease or other bacterial lesions and those occurring in autoimmune diseases. The main clinical conditions and specific therapeutic intervention options for each biological phenotype of calcification are also examined and discussed.

Structural Heart Disease

Cardiovascular (CV) calcification is a growing research topic in cardiology, mainly because calcium salt deposition is associated with major CV diseases such as atherosclerosis, valvular diseases, and several hypertrophic cardiomyopathies. Recently, coronary artery calcium measurements have been suggested to be the most accurate screening or risk assessment tool for atherosclerotic CV disease [1].

Calcification can involve the arteries and heart valves, causing stiffness and dysfunction, and less commonly the myocardium, causing fibrosis, conduction defects, and pericarditis. Figure 1 shows schematically the most common pathologic calcifications in the heart and vascular system, the two most important being vascular and valvular calcifications. Although risk factors and similar molecular pathways are shared, vascular and valvular calcification occur in different tissues, respond to different stimuli, and represent two distinct biological phenotypes [2].

There are also differences between vascular calcifications in terms of whether calcium deposition occurs predominantly in the intimal or medial layer of the arterial wall.

This article summarizes the intracellular processes and pathways that control hyperphosphatemic calcification, which occurs mainly in the vascular media, and intimal vascular calcification, which is mainly associated with inflammation. The specific mechanisms of both processes are analyzed in two key regions, namely the arterial wall and the aortic valve. Molecular mechanisms leading to less frequent calcification in response to infections and autoimmune diseases are also being investigated. Finally, we consider

Calcium In Arteries: Why Does Calcium Build Up In Arteries And How To Reduce It?

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