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Cardiovascular disease(CVD) is the leading cause of death worldwide, and is closely interconnected with other cardiovascular, renal and metabolic (CVRM) conditions.1,2
What is CVD?
CVD consists of a group of heart and blood vessel disorders and cardiovascular (CV) conditions which can include heart failure (HF), amyloidosis, atherosclerotic cardiovascular disease (ASCVD), coronary heart disease (CAD) and dilated cardiomyopathy (DCM).1,3-5 In addition to being genetically predisposed to CVD, biological risk factors such as high blood pressure, high cholesterol levels, and elevated blood glucose can contribute to the development of CVD.6 Lifestyle factors, including diet, lack of physical activity, and tobacco or alcohol use, also play a significant role.1
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Approximately one in three
patients with chronic coronary syndromes will also have type-2 diabetes (T2D).7
Risk of experiencing a major CV event doubles
for people living with both CAD and T2D, compared with those diagnosed with T2D alone.8
Risk factors including chronic kidney disease (CKD)
also increase the chances of someone having an additional CV event, such as a heart attack.9
[#news]
[#CVD]
Types of CVD
Data from 2019 states that approximately 523 million people across the world live with CVD, often with declining CV health.10 Not only is CVD the leading cause of death worldwide, it also includes many conditions that are often interlinked such as: 1,2
HF
HF is a complex syndrome that occurs when the heart cannot pump enough blood around the body,11 and is often complicated by multiple interrelated diseases that have clear cardiometabolic and cardiorenal interconnections.12,13
While patients with chronic HF may have similar symptoms, ultrasound scans of their heart show different types of disease.14,15 Risk factors for HF include aging, family history of HF, unhealthy living habits, obesity, high blood pressure, and diabetes.16
ASCVD
ASCVD involves the buildup of plaque in artery walls that can result in a heart attack, angina (stable or unstable), stroke, transient ischaemic attack (TIA) or aortic aneurysm.17,18 Risk factors for ASCVD include high cholesterol and triglyceride levels, hypertension, and type 1 (T1D) and T2D as well as lifestyle factors such as smoking, lack of physical activity, and diet high in saturated fat.19,20 It is the most common clinical consequence of dyslipidaemia and is associated with abnormal lipid markers.21 In 2022, it is estimated that almost 19 million adults in the United States had ASCVD.22
CAD
CAD is a chronic and persistent condition in which the arteries that supply the heart with blood are narrowed.17,23 Atherosclerotic plaque, a build-up of deposits of fatty material, cholesterol, cellular waste products and other substances, accumulate in the coronary arteries, obstructing the blood flow to the heart muscle.17 The plaque can cause partial or complete blockage of blood supply to the heart muscle, which can cause a heart attack.17,23 Risk factors for CAD include age, gender, ethnicity and family history, as well as hypertension, hyperlipidaemia, diabetes, and obesity.24 In one study, approximately one in three patients with chronic coronary syndromes also had T2D and these patients are at increased risk for a major adverse CV event.7 CAD can weaken the heart muscle over time, which can lead to HF.25,26
For those who survive a heart attack, it may often be the start of a journey into declining CV health. According to a study conducted in Finland, over 30% of those who have had a heart attack go on to have a subsequent attack, stroke or death within the first year, underlining the importance of early diagnosis, developing treatments to reduce or stop coronary heart disease progression, and addressing uncontrolled risk factors.27
DCM
(DCM) is a form of CVD characterized by the enlargement and weakening of the heart's ventricles, including the left ventricle. As a type of heart muscle disease, DCM disrupts the heart's ability to pump blood effectively throughout the body. Unlike other CVdiseases, it is not caused by CAD, hypertension, valvular disease, or congenital heart defects. DCM can arise from various factors, including genetic mutations, viral infections, autoimmune diseases, and exposure to toxins.5 This condition often progresses to HF, a severe form of CVD, due to the heart's compromised function.5
Patients with DCM may experience symptoms common to CV diseases, such as fatigue, shortness of breath, swelling in the legs and abdomen, and irregular heartbeats. These symptoms reflect the heart's reduced capacity to circulate blood efficiently. The risk of complications, including HF and sudden cardiac death, is significant, making it a serious health concern.5 DCM can profoundly impact a patient's quality of life, limiting physical activity and increasing the need for medical interventions.5
The prognosis for DCM varies depending on the underlying cause and the effectiveness of treatment strategies, highlighting the importance of early detection and management within the broader context of CVD prevention and care.5
[#CVrisks]
Managing residual CV risks
Residual CVD risk is the risk of occurrence of CVD events despite receiving treatment for or achieving targets for risk factors such as low density lipoprotein (LDL) cholesterol, blood pressure, and glycemia.28,29 In 2019, nearly 50% of all US adults have some type of CVD and current treatments may only prevent up to 50% of CVD events in patients with diabetes.28,30-32 Some of the factors that can impact residual CVD risk are high levels of aldosterone, dyslipidaemia, and hypertension.33,34
Hypertension
Hypertension, or high blood pressure, is a common condition that relates to increased force of the blood pushing against the blood vessel walls.35 Risk factors for hypertension include kidney disease and potentially genetic factors.36,37 It is sometimes referred to as a silent killer as patients frequently do not experience obvious symptoms, although the condition is actively deteriorating the overall health of the individual:35
- High blood pressure can lead to damage in multiple organs (this is called “end-organ damage”), which is often associated with the heart, as your heart needs to work harder to pump blood.35
- Other organs can also be impacted, including your kidneys because the small vessels in the kidneys are affected, your eyes, and even your brain vessels.35,38
Normal blood pressure is defined as 120 mmHg or less for the systolic measurement, and 80 mmHg or less for the diastolic measurement.39 Individuals with hypertension have consistently elevated blood pressure levels, which may remain high despite lifestyle changes and medications. This condition is classified into uncontrolled hypertension (uHTN), where blood pressure remains high despite treatment and resistant hypertension (rHTN), where blood pressure fails to normalize despite the use of three or more antihypertensive medications from different classes.40,41
Elevated blood pressure affects an estimated 1.3 billion people worldwide,35 and is the second leading cause of kidney failure in the US, following diabetes, causing 27% of cases. Patients with resistant hypertension (https://www.astrazeneca.com/our-therapy-areas/cardiovascular-renal-and-metabolism/renal.html) face a higher risk of CV and renal adverse events compared with patients with more easily controlled hypertension.42,43
Aldosterone is a steroid hormone made by the adrenal gland that controls the balance of water and salts in the kidney and is part of the renin-angiotensin-aldosterone system (RAAS) that helps to regulate blood pressure, electrolyte balance, and fluid balance in the body.44,45 Aldosterone performs this function by keeping salt in the body while facilitating the removal of potassium. Excessive aldosterone production is associated with hypertension and several cardiorenal diseases, including CKD and CAD.44 It can also have off-target effects, such as in the endothelium where elevated aldosterone levels are correlated with increased inflammatory markers, stimulating fibrosis in the kidney, heart, and other vessels,33,46 and to increased cardiorenal risk and the subsequent dysfunction resulting in end-organ damage that is independent of hypertension.4944-47
Blocking the aldosterone pathway has been shown to be very effective in patients with hypertension that is difficult to control.48
Dyslipidaemia
Dyslipidaemia, which can be the result of lifestyle or genetic factors, occurs when there are abnormal levels of lipids (such as cholesterol [LDL-C, HDL-C, and total] or triglycerides) in the bloodstream.49 Lipids are absorbed from the intestines and carried throughout the body via lipoproteins and are used for energy, steroid production, or bile acid formation.49 Risk factors for dyslipidaemia include genetic predisposition, lifestyle, obesity, diabetes mellitus, CKD, hypothyroidism, and liver disease.49 Though dyslipidaemia is typically asymptomatic, it can be detected with a blood test measuring lipid levels. In the long term, chronic inflammation can induce dyslipidaemia, which is a significant risk factor for CV diseases, including atherosclerosis and other CV complications. 49,50
High levels of LDL-C are estimated to cause 2.6 million deaths worldwide every year.51 According to a case-control study from Jakarta, when accompanied by comorbidities like hypertension, dyslipidaemia becomes a significant risk factor for CVD.52 Based on a cross-sectional study across Europe, despite high-intensity statin therapy, over half of high-risk CVD patients struggle to achieve their LDL-C targets, highlighting the need for more effective therapies.53
Dyslipidaemia, including hypercholesterolaemia, is associated with poor outcomes such as stroke and myocardial infarction (MI). The impact of elevated LDL-C has escalated from being the 15th leading cause of death in 1990 to the 8th in 2019. Effective LDL-C lowering therapies have been shown to improve global CVD outcomes by preventing or delaying disease onset and reducing the risk of serious CV events in patients with existing CVD.54
[#collaborations]
Collaborations to support CV care
We are proud to be working with HCPs, patients, governments and policy makers to improve access to healthcare, remove barriers to diagnosis and optimal treatment, changing how CVRM diseases are detected, diagnosed and treated to accelerate medical practice change together to make a difference for patients.
[#ourpeople]
Our people
Built on an impressive legacy in CVRM research, we are uniquely positioned to build a healthier and longer future for people with these diseases. Our team of over 1,000 people spans more than 23 functions including early and late R&D, medical and commercial.
Our employees are accomplished and experienced scientists, researchers, clinicians, and healthcare and commercial professionals dedicated to advancing novel science and driving practice change to benefit patients with CVRM diseases.
References
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Veeva ID: Z4-66920
Date of preparation: March 2025