Harmonization of the American College of Cardiology/American Heart Association and European Society of Cardiology/European Society of Hypertension Blood Pressure/Hypertension Guidelines: Comparisons, Reflections, and Recommendations

Actually, You Can Catch Up On Sleep

August 30, 2024 8:00 AM EDT

If you're like most Americans, you're not getting enough sleep.  And that exacts a toll on the body—especially the heart.  Poor sleep has been linked to high blood pressure, high cholesterol, inflammation, heart attack, and more. 

One solution: catch up on your sleep when you can, especially on weekends. But while that may help you feel more rested, can it really undo the cardiac damage that comes from a sleep-poor work week? According to a new study to be presented at the Sept. 1 meeting of the European Society of Cardiology, it may. 

The findings come from an analysis of nearly 91,000 people enrolled in the UK Biobank project, a large-scale biomedical database. People reported how much sleep they got per night, and those averaging fewer than seven hours—about 22% of the sample group—were considered sleep-deprived. People in the study briefly wore sleep-tracking devices that allowed the investigators to measure how much additional sleep they got over the weekend. The researchers then followed up on participants' cardiovascular health 14 years later.

Read More: Cuddling Might Help You Get Better Sleep

Sleep-deprived people who got the most compensatory weekend sleep—sleeping at least 90 minutes more than they usually did during the week—had about a 20% lower risk of various illnesses, including heart failure, atrial fibrillation, ischemic heart disease, and stroke, compared to people who slept the least on weekends. 

Weekend catch-up sleep may have these effects in multiple ways. Heart rate slows during sleep and blood pressure can fall by 10% to 20%, a phenomenon known as nocturnal dipping. Poor sleep can also lead to chronic inflammation, which helps give rise to circulatory plaques, and catching up on sleep helps alleviate that. According to the University of Chicago School of Medicine, adults who sleep less than five hours a night also have a 200% to 300% increased risk of coronary artery calcification. Type 2 diabetes and obesity are linked to too little sleep as well, imposing their own strain on the heart. 

"Our results show that for the significant proportion of the population in modern society that suffers from sleep deprivation, those who have the most 'catch-up' sleep at weekends have significantly lower rates of heart disease than those with the least," said study co-author Zechen Liu, of Beijing's National Center of Cardiovascular Disease, in a statement.    

New Chronic Coronary Syndrome Guidelines Expand Diagnostic Tools And Ways To Prevent Major Adverse Events

The 2024 European Society of Cardiology (ESC) Guidelines on the management of chronic coronary syndromes (CCS) include a focus on both larger and smaller blood vessels of the heart; new models to estimate chances of blocked large arteries (so-called obstructive coronary artery disease); optimal selection and sequence of tests; drugs and interventions to prevent disease complications and improve symptoms, and the fundamental role of patient involvement.

"The new guidelines prompt cardiologists to rethink chronic coronary syndromes as caused not only by blockages in large arteries but also by dysfunction of smaller vessels (microcirculation)," explains Guidelines co-chair Professor Christiaan Vrints, Antwerp University Hospital and University of Antwerp, Antwerp, Belgium.

"Over half of individuals suspected of CCS may have angina/ischemia with nonobstructive coronary arteries (ANOCA/INOCA) caused by coronary artery spasm or microcirculatory dysfunction. This condition is often missed—on average it is diagnosed only after seeing three cardiologists—because the usual tests don't work well to detect it. Patients may suffer severely from persistent symptoms that can cause repeated hospitalizations and even heart failure."

Published in the European Heart Journal, the guidelines highlight that persistently symptomatic patients with suspected ANOCA/INOCA who do not respond to guideline-derived medical therapy should undergo invasive coronary functional testing to determine underlying endotypes and to guide appropriate medical therapy.

A further new recommendation strongly endorsed by the guidelines is the use of the risk factor-weighted clinical likelihood model to estimate the pre-test likelihood of obstructive coronary artery disease. With this new prediction model, around half of individuals assessed for chest pain have a very low likelihood of large artery blockage (</=5%), and in these patients further testing should be deferred, whereas with the ESC 2019 model, only 19% were identified as having a very low likelihood. This prediction model has been developed and validated in Western countries (northern EU, UK, and US). The results may vary depending on region, race, cultural differences, and healthcare system organisations.

For individuals with symptoms suggestive of chronic coronary syndrome who have a low to moderate (>5%–50%) likelihood of obstructive coronary artery disease based on symptoms, age, sex and risk factors, coronary computed tomography angiography (CCTA) is very effective in ruling out coronary atherosclerosis, or at the other extreme, in estimating the risk of major adverse cardiovascular events based on disease anatomy.

"Rarely, however, is a single non-invasive test sufficient to diagnose obstructive disease of the epicardial coronary arteries and a sequential approach is required. When CCTA reveals coronary blockages of intermediate severity, additional tests like stress echocardiography, stress positron emission tomography or stress cardiac magnetic resonance perfusion imaging, if available, are recommended to evaluate the functional significance of the blockages. These additional exams also help to diagnose ANOCA/INOCA when CCTA does not reveal any blockages," explains Professor Vrints.

"In patients with large coronary artery blockages, surgical or percutaneous revascularization is recommended for specific anatomical and/or clinical groups of patients in whom revascularization over medical therapy alone has been shown to prolong survival and to reduce deaths from cardiovascular causes, as well as spontaneous myocardial infarctions and symptoms caused by cardiac ischemia," says guidelines co-chair Professor Felicita Andreotti, Fondazione Policlinico Universitario Gemelli IRCCS and Catholic University Medical School, Rome, Italy.

Prof. Andreotti adds that representatives of the European Association for Cardio-Thoracic Surgery (EACTS) and representatives of the Patient Forum were included in the 28-member task force and that the Guidelines have been endorsed by the EACTS.

The indications for coronary revascularization in the 2024 Guidelines are largely similar to those of 2018: namely, symptoms related to ischemia that are refractory to medical therapy alone, and/or significant disease of the left main stem, of the proximal left anterior descending artery, or of multiple large epicardial arteries.

The Guidelines state/recommend that the most appropriate revascularization modality should be selected based on the patient's profile, coronary anatomy, procedural factors, patient preferences and outcome expectations. Surgery, if possible, is preferred over percutaneous coronary intervention in patients with extensive disease, especially those with diabetes or reduced left ventricular ejection fraction.

When performing revascularization via percutaneous coronary intervention, intracoronary imaging, in addition to pressure measurements, is helpful to guide interventions and enhance immediate and long-term results, especially in complex anatomical scenarios such as left main disease, bifurcations, or long lesions.

"Percutaneous coronary intervention using modern thin-strut stents allows patients who are not at high ischemic risk and/or who are at high bleeding risk to safely shorten the duration of dual antiplatelet therapy. In all or in certain subgroups of patients with chronic coronary syndromes, new lipid-lowering, metabolic and anti-inflammatory medical strategies have the potential to lower the risk of adverse cardiovascular events," adds Professor Andreotti.

"Patient education and involvement in decision-making and self-care, along with mobile-health interventions and simplified medication regimens, have the potential to improve adherence to healthy lifestyles and to medical therapy, and to enhance long-term patient monitoring for disease complications and side effects of treatment," explains Professor Vrints.

The Guidelines co-chairs conclude, "Chronic coronary syndromes are a global health concern because transient or long-lasting damage of the heart caused by diseases of the coronary circulation can cause ineffective heart pump function or malignant arrhythmias that can be fatal. Coronary syndromes remain the single largest cause of death in the adult population worldwide, resulting in millions dying every year. Therefore, the new guidelines stress the importance of early detection, appropriate treatment, and careful long-term follow-up."

More information: 2024 ESC Guidelines for the Management of Chronic Coronary Syndromes, European Heart Journal (2024). DOI: 10.1093/eurheartj/ehae177

Citation: New chronic coronary syndrome guidelines expand diagnostic tools and ways to prevent major adverse events (2024, August 30) retrieved 30 August 2024 from https://medicalxpress.Com/news/2024-08-chronic-coronary-syndrome-guidelines-diagnostic.Html

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Study Finds New Source Of Cardiac Inflammation

Globally, ischemic heart disease is the leading cause of death. A myocardial infarction (MI), commonly referred to as a "heart attack," is the first event in which insufficient coronary blood flow results in the death of a portion of the heart. Heart failure, heart wall remodelling, and severe inflammation result from this.

Surprisingly, anti-inflammatory medications have not been able to stop heart failure. They are therefore not a standard component of post-MI care. The most effective cellular and molecular targets for inflammation, however, might still be unidentified.

In the Aug. 28, 2024 issue of Nature, researchers from University of California San Diego in the laboratory of Dr. Kevin King, associate professor of bioengineering and medicine, and a cardiologist at the Sulpizio Cardiovascular Center, report the discovery of a novel mechanism of cardiac inflammation that may expand therapeutic opportunities to prevent heart attacks from becoming heart failure.

Inflammation after MI is classically credited to professional immune cells like neutrophils and macrophages that infiltrate the infarcted heart and respond to molecules in the debris of dying cells. So the team was surprised when they discovered that the proinflammatory "type I interferon (IFN) response" was activated, not in the infarct where immune cells were concentrated, but instead in the borderzone, surrounding the infarct.

The borderzone has been a fascinating yet understudied area of the infarcted heart. It is where surviving heart muscle cells attempt to stabilize and even proliferate after being disconnected from their dying neighbor cells. Unfortunately, the borderzone has proven a challenging region to study because it is not easily isolated from the rest of the heart. Researchers overcame this obstacle using methods they recently reported based on single cell RNAseq and spatial transcriptomics where cells of the borderzone are recognized based on their patterns of gene expression.

To determine which cell type initiates borderzone inflammation, the team created a library of conditional knockout mice, each unable to initiate IFN signaling in a different cell type. To their surprise, heart muscle cells called cardiomyocytes emerged as the dominant initiators of borderzone IFN signaling. They found that mechanically stressed cardiomyocytes in the borderzone frequently suffered nuclear envelope rupture, which allowed escape of nuclear DNA and sensing by cytosolic DNA sensors, leading to activation of IFN signaling. This in turn caused mechanical weakening of the heart wall and made it vulnerable to dilation, thinning, and rupture, providing a mechanistic explanation for the team's previous reported observation that mice lacking IFN responses exhibited improved survival after MI.

"In the hospital, we care for patients with heart attacks and heart failure every day. New therapeutic targets for MI with the potential to prevent development of heart failure are incredibly important, said Dr. King, senior author of the study an on the faculty in the Shu Chien Gene Lay Department of Bioengineering and the Division of Cardiology at UC San Diego.

Many questions remain, however the newly reported findings suggest that limiting mechanical stress at the borderzone, inhibiting DNA sensing, and preventing type I IFN signaling may represent new opportunities for patients to avoid development of heart failure after MI. (ANI)

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