Ischemic heart disease is a major cause of death and disability worldwide, while angina (short for “angina pectoris”) represents its most common symptom.1 Angina has been shown to double the risk of major cardiovascular events.2 Every year in Europe, 4.1 million deaths occur due to coronary artery disease (CAD), with 82% of these deaths in people older than 65 years.1
The annual incidence, or number of new cases diagnosed, of angina is 1% for the Western male population aged 45–65 years. The incidence is slightly higher in women. The number of cases increases with age in both genders. Patients with angina begin to be diagnosed at 65 years old for men and 70 years old for women.
The incidence and prevalence of patients with angina is anticipated to increase in the coming decade as a result of aging populations, more wide-spread use of life-prolonging therapies, and the better management of acute coronary syndromes3, as well as the obesity epidemic. Angina also has a negative impact on quality of life and leads to a threefold higher risk of disability7, a risk of losing their jobs that is 1.5 times higher7, and a fourfold higher risk of depression.8
30,000 – 40,000
cases of angina per million in Western countries4
1.6 %
of the world’s population suffers from angina pectoris
5
60%
of angina patients are not receiving an optimal medical therapy6
The multiple faces of angina
Angina is a pain or discomfort in the chest caused by the insufficiency of oxygen in the cardiac cells. It often has a squeezing or pressure-like feel in the chest and usually lasts for no more than 2 to 10 minutes. Angina typically meets the following criteria: characteristic chest pain in terms of quality and duration, brought about by physical exertion or emotional stress. It is usually relieved by rest and/or nitrates within minutes.1
Many angina patients suffer from atypical angina. These patients do not have typical chest pain and may complain about shortness of breath, excessive sweating, extreme fatigue, pain at a site other than the chest, a sensation of indigestion or discomfort in the upper part of the abdomen. This complicates diagnosis of angina pectoris and contributes to it being frequently poorly recognized by physicians and misinterpreted by patients.9
77%
of recently-diagnosed patients present with atypical angina pectoris9.
Thorough history-taking during an appointment with your doctor remains the cornerstone for diagnosing chest pain. Tests are often necessary to confirm the diagnosis.1
What causes angina?
An in-depth understanding of the pathophysiology of angina is essential for timely diagnosis and optimal management. In many patients, the underlying pathology is atherosclerotic narrowing or obstruction of one or more major coronary arteries. This reduces blood flow to the heart muscle, causes a mismatch between the oxygen demand and delivery, leading to angina attacks.1
Angina may also occur in the absence of coronary artery disease and obstructive lesions, or even in the presence of normal coronary arteries.1 The underlying mechanisms of angina in these patients are the functional alterations of the coronary circulation at the level of the coronary microcirculation.1
This is actually not a rare situation. In some registries, almost two-thirds of newly-diagnosed patients don’t have significant coronary obstructions11, which makes clarification of the underlying mechanisms of angina even more important.
How is angina pectoris treated?
Strategies to improve management of angina remain a priority for health care professionals in order to decrease the risk of major cardiovascular events and mortality.
Implementing healthy lifestyle behaviors is an indispensable part of managing angina pectoris. This includes quitting smoking, getting regular physical activity, adopting a healthy diet, and maintaining a healthy weight. Such lifestyle changes could significantly decrease the risk of future cardiovascular events and death. Benefits after implementing healthier lifestyle behaviors are evident as early as 6 months.12
When it comes to the medical therapy, current guidelines recommend conservative antianginal treatment to control symptoms, prior to invasive coronary artery revascularization.9
Clinical studies have demonstrated that coronary revascularization is not superior to optimal medical therapy in patients with stable angina. The recent ISCHEMIA study confirmed that an initial invasive strategy did not reduce the risk of ischemic cardiovascular events or death from any cause compared to medical therapy alone. That is why pharmacological treatment intensification is recommended as a first step for angina patients prior to an invasive strategy.13
AND SERVIER?
Fourth leading global pharmaceutical group in cardiology worldwide and second in Europe*, Servier has been involved in cardiovascular disease treatments for more than 60 years. We aim to maintain our position through strategic and innovative life cycle management (LCM) to capitalize on our expertise in incremental innovation, particularly in the development of Single Pill Combinations (SPC). SPCs are medicines combined in a single tablet, which simplify treatment, thereby promoting better adherence.
Servier, with World Heart Federation, the principal representative body for the global cardiovascular community, and Global Heart Hub, the foremost association for patients with CVD, produces campaigns to raise public awareness of the symptoms of angina, which are often underestimated.
The MyHealthPartner website has been developed by Servier and offers a wealth of certified information on chronic diseases such as angina. It enables patients to better understand their pathologies, associated risk factors, and symptoms.
*IQVIA, Analytics Link / World 74 countries – MAT Q3-2021
KEY TAKEAWAYS
1. Balla C, Pavasini R, Ferrari R, Cardiology 2018;140:52–67.
2. Mozaffarian D et al. Circulation. 2016; 33(4): e38-e360.
3. Ohman EM. N Engl J Med. 2016; 374:1167-1176.
4. Maddox TM, Reid KJ, Spertus JA, et al: Angina at 1 year after myocardial infarction: prevalence and associated findings. Arch Intern Med 2008; 168: 1310–1316.
5. Vos T et al. Lancet.2012;380(9859):2163-2196.
6. Alexander KP et al. Interact J Med Res. 2016;5(2): e12.
7. Padala SK et al. J Cardiovasc Pharmacol Ther. 1074248417698224 2017 Jan 01.
8. Jespersen L et al. Clin Res Cardiol. 2013; 102: 571-58.
9. Douglas PS et al. N Engl J Med. 2015;372:1291-1300.
10. Ambrosio G et al. 2019;70(5):397-406.
11. Westermann D. J Clin Exp Cardiol. DOI:10.4172/2155-9880.1000387
12. Knuuti J et al. Eur Heart J. 2020; 41(3):407-477.
13. Maron J et al. N Engl J Med. 2020; 382:1395-1140.