Informação da revista
Vol. 43. Núm. 3.
Páginas 159-162 (março 2024)
Partilhar
Partilhar
Baixar PDF
Mais opções do artigo
Vol. 43. Núm. 3.
Páginas 159-162 (março 2024)
Editorial comment
Acesso de texto completo
Refining the classification of cardiovascular prevention
Aperfeiçoando a classificação de prevenção cardiovascular
Visitas
1255
Rui Azevedo Guerreiro
Hospital CUF Descobertas, Cardiology, Lisbon, Portugal
Este item recebeu
Informação do artigo
Texto Completo
Bibliografia
Baixar PDF
Estatísticas
Figuras (1)
Texto Completo

The prevention of coronary artery disease (CAD) is a critical focus area in cardiology. As per the 2021 European Society of Cardiology (ESC) guidelines on cardiovascular disease prevention in clinical practice,1 the current definition of prevention is a binary variable. It categorizes individuals into two groups: those aiming to prevent their first myocardial infarction (MI) (primary prevention), and those who have already experienced a MI and are now aiming to prevent a second one (secondary prevention).

However, certain healthcare experts in disease prevention2,3 argue that this classification of cardiovascular prevention as solely primary and secondary is overly simplistic. They believe that this approach fails to capture the true complexity of the subject, with significant implications in terms of how cardiologists diagnose and treat CAD.

Instead, a more comprehensive classification system can be employed to describe cardiovascular prevention. This system involves four distinct categories3: primordial, primary, secondary, and tertiary prevention (Figure 1).

Figure 1.

Stages in the prevention of cardiovascular disease.

(0.39MB).

Primordial prevention is a vital component of cardiovascular disease prevention as it aims to halt the development of cardiovascular risk factors in the general population. The strategies employed in primordial prevention encompass multifaceted approaches such as advocating for a healthy diet, promoting lifestyle modifications such as regular exercise, discouraging smoking, and reducing harmful environmental exposure.2

Primary prevention is centered around individuals who have cardiovascular risk factors but have not yet manifested any evidence of CAD or in whom CAD has not been diagnosed. Similarly to primordial prevention, primary prevention strategies prioritize lifestyle modifications and dietary adjustments to manage risk factors such as hypertension, dyslipidemia, obesity and diabetes. These lifestyle changes include adopting a healthy diet, engaging in regular exercise, maintaining a healthy weight, and managing stress. In addition, pharmacological interventions, such as statins or antihypertensive drugs, could be prescribed, tailored to the individual's specific risk profile. By combining lifestyle modifications with appropriate medication, the primary prevention approach aims to significantly reduce the occurrence of cardiovascular events in individuals at risk.2

Secondary prevention concentrates on diagnosing subclinical asymptomatic CAD. The objective of secondary prevention is to identify individuals at high risk for cardiovascular events through screening methods, which enable the early detection of subclinical CAD. Once this is diagnosed, prompt intervention and implementation of appropriate strategies become crucial in controlling cardiovascular risk factors and minimizing the progression of the disease. Management strategies in secondary prevention encompass lifestyle modifications, similar to primary prevention. Medications are often prescribed to manage specific risk factors, including antiplatelet agents. While their utility in primary prevention is limited,4,5 more substantial evidence supports their effectiveness in secondary prevention.6 Close monitoring of the patient's condition and more regular follow-up visits enable healthcare providers to adjust interventions and optimize risk factor control, thus reducing the likelihood of future cardiovascular events.2

Tertiary prevention focuses on preventing additional cardiovascular events after the occurrence of an initial event. This stage emphasizes comprehensive strategies aimed at reducing morbidity and mortality associated with CAD. It involves a combination of approaches, including coronary revascularization procedures such as angioplasty or bypass surgery; cardiac rehabilitation programs, providing structured exercise training, education, and support to enhance cardiovascular health; and medications, including antiplatelet agents, statins, beta-blockers, and angiotensin-converting enzyme inhibitors, to prevent recurrent events and maintain optimal cardiovascular function. Tertiary prevention ensures that individuals who have experienced a cardiovascular event receive appropriate interventions and support to minimize the risk of future events and achieve the best possible outcomes.2

By adopting this enhanced approach, healthcare professionals, including cardiologists, can better understand and address the multifaceted nature of CAD prevention.

In light of this classification of preventive cardiology, how can we improve patient care and decrease the prevalence of patients in tertiary prevention?

Regarding primary prevention, evidence suggests that patients’ cardiovascular risk factors are not adequately controlled. The primary care arm of EUROASPIRE V7 assessed 2759 individuals (57.6% women, mean age 59 years) without previous manifestations of atherosclerotic cardiovascular disease. These individuals had been on blood pressure- or cholesterol-lowering medications for at least six months before the study interview. The findings revealed that 18% of participants were smokers, 43.5% were obese, and among those on blood pressure medications, only 47% achieved target levels of <140/90 mmHg (or <140/85 mmHg for diabetics). Furthermore, of those taking lipid-lowering agents, only 46.9% achieved low-density lipoprotein (LDL) cholesterol levels below 100 mg/dl. The prevalence of self-reported diabetes was 35.8%, and approximately one in three individuals had glycated hemoglobin levels of 7.0% or higher. Only 36.4% engaged in regular exercise, while nearly 40% were entirely sedentary.7 In light of these results, it is evident that greater attention and efforts are required to optimize primary prevention strategies and ensure effective control of patients’ cardiovascular risk factors.

Regarding secondary prevention, both general practitioners and cardiologists should prioritize the diagnosis of subclinical CAD as a crucial aspect of cardiovascular care, if we wish to reduce the incidence of MI, prevent sudden cardiac death, and have a meaningful effect on cardiovascular prevention. Each patient in tertiary prevention represents a missed opportunity for preventive cardiology.

The advent of cardiac computed tomography (CT) has revolutionized secondary prevention. Previously available diagnostic exams such as treadmill stress testing, stress echocardiography, and myocardial perfusion scintigraphy could only detect obstructive CAD with blood-flow limiting lesions and subsequent myocardial ischemia. However, cardiac CT has made it possible to identify non-obstructive subclinical coronary atherosclerosis.

The coronary artery calcium (CAC) score, obtained through non-contrast cardiac CT, is an affordable and non-invasive imaging technique that provides a personalized assessment of atherosclerotic burden. It reflects an individual's cumulative lifetime risk factor exposure, which cannot be easily obtained from serum markers or other cardiac imaging methods.8

The Multi-Ethnic Study of Atherosclerosis (MESA),9 Heinz Nixdorf Recall10 and EISNER11 studies, as well as ongoing studies such as CorCal (NCT03439267) and ACCURATE (NCT03972774), are shedding light on the potential benefits of using CAC scoring as a screening tool for CAD, similar to how mammography is used for breast cancer screening.12

The MESA cohort, consisting of asymptomatic individuals without prior coronary heart disease, showed that even mild calcification (CAC score 1–100) significantly increases the risk of coronary heart disease compared to those with no calcification, with a hazard ratio of 3.61 (95% confidence interval [CI] 1.9–6.7).9 Furthermore, among individuals in the MESA study with normal LDL cholesterol levels, the presence of any CAC remains strongly associated with an elevated risk of coronary heart disease events, with a hazard ratio of 6.65 (95% CI 2.99–14.78).13

A CAC scan revealing zero coronary calcification serves as a powerful negative risk factor for CAD. It effectively reclassifies a significant number of individuals from intermediate- to low-risk categories, allowing for the implementation of conservative treatment strategies.14,15 A comprehensive meta-analysis incorporating data from 13 studies and over 71595 asymptomatic subjects confirmed that individuals with a CAC score of 0 have a relative risk of 0.15 (95% CI 0.11–0.21) for suffering a cardiovascular event compared to those with any CAC.16 Additionally, in a cohort of 44052 asymptomatic patients, a CAC score of 0 was associated with less than 1% 10-year risk of all-cause mortality, indicating an excellent long-term prognosis.17 These robust findings further support the potential of the CAC score as a valuable tool in cardiovascular risk assessment across diverse patient populations, including women, diabetic patients, and the elderly.13–16

Patients who had a higher than expected CAC score and were reclassified into high- or very-high cardiovascular risk groups are more likely to adhere to statin therapy18 and antihypertensive medications.11 The visual representation of CAC scores may act as a powerful motivator for patients, increasing their perceived cardiovascular risk and encouraging them to adhere to medications and adopt healthier lifestyles.

In the early stages of CAC scoring, there were concerns regarding radiation exposure. However, with advancements in modern testing equipment, the median radiation exposure associated with CAC scoring is approximately 1 mGy.19 This level of exposure is significantly lower than the mean of 4.15 mGy to the breast from a digital mammography, as identified in the Digital Mammographic Imaging Screening Trial conducted by the American College of Radiology Imaging Network.20

The importance of CAC scoring in secondary prevention led to the 2021 ESC guidelines on cardiovascular disease prevention in clinical practice1 recommending that CAC scoring may be considered to improve risk classification around treatment decision thresholds (class IIb, level of evidence B). The more recent 2022 Portuguese Society of Cardiology consensus document on chronic coronary syndrome assessment and risk stratification in Portugal6 recommends CAC scoring for every asymptomatic adult over 40 years old with moderate cardiovascular risk (SCORE ≥1%–<5%).

In conclusion, the classification of cardiovascular prevention into primordial, primary, secondary, and tertiary prevention provides a comprehensive framework for better addressing the treatment of CAD. To improve patient care and to reduce the number of patients in tertiary prevention, both optimizing the control of cardiovascular risk factors in primary prevention and diagnosing subclinical CAD in secondary prevention are crucial to reduce the burden of CAD.

Conflicts of interest

The author has no conflicts of interest to declare.

References
[1]
F.L.J. Visseren, F. Mach, Y.M. Smulders, et al.
2021 ESC Guidelines on cardiovascular disease prevention in clinical practice.
Eur Heart J, 42 (2021), pp. 3227-3337
[2]
D. Capodanno, D.L. Bhatt, J.W. Eikelboom, et al.
Dual-pathway inhibition for secondary and tertiary antithrombotic prevention in cardiovascular disease.
Nat Rev Cardiol, 17 (2020), pp. 242-257
[3]
L.A. Kisling, J.M. Das.
Prevention strategies.
StatPearls Publishing, (2023),
[4]
J.M. Gaziano, C. Brotons, R. Coppolecchia, et al.
Use of aspirin to reduce risk of initial vascular events in patients at moderate risk of cardiovascular disease (ARRIVE): a randomised, double-blind, placebo-controlled trial.
Lancet, 392 (2018), pp. 1036-1046
[5]
J.J. McNeil, M.R. Nelson, R.L. Woods, et al.
Effect of aspirin on all-cause mortality in the healthy elderly.
N Engl J Med, 379 (2018), pp. 1519-1528
[6]
N. Bettencourt, L. Mendes, J.P. Fontes, et al.
Consensus document on chronic coronary syndrome assessment and risk stratification in Portugal: a position paper statement from the [Portuguese Society of Cardiology's] Working Groups on Nuclear Cardiology, Magnetic Resonance and Cardiac Computed Tomography, Echocardiography, and Exercise Physiology and Cardiac Rehabilitation.
Rev Port Cardiol, 41 (2022), pp. 241-251
[7]
K. Kotseva, G. De Backer, D. De Bacquer, et al.
Primary prevention efforts are poorly developed in people at high cardiovascular risk: a report from the European Society of Cardiology EURObservational Research Programme EUROASPIRE V survey in 16 European countries.
Eur J Prev Cardiol, 28 (2021), pp. 370-379
[8]
S.P. Whelton, K. Nasir, M.J. Blaha, et al.
Coronary artery calcium and primary prevention risk assessment: what is the evidence? An updated meta-analysis on patient and physician behavior.
Circ Cardiovasc Qual Outcomes, 5 (2012), pp. 601-607
[9]
R. Detrano, A.D. Guerci, J.J. Carr, et al.
Coronary calcium as a predictor of coronary events in four racial or ethnic groups.
N Engl J Med, 358 (2008), pp. 1336-1345
[10]
R. Erbel, S. Mohlenkamp, S. Moebus, et al.
Coronary risk stratification, discrimination, and reclassification improvement based on quantification of subclinical coronary atherosclerosis: the Heinz Nixdorf Recall study.
J Am Coll Cardiol, 56 (2010), pp. 1397-1406
[11]
A. Rozanski, H. Gransar, L.J. Shaw, et al.
Impact of coronary artery calcium scanning on coronary risk factors and downstream testing the EISNER (Early Identification of Subclinical Atherosclerosis by Noninvasive Imaging Research) prospective randomized trial.
J Am Coll Cardiol, 57 (2011), pp. 1622-1632
[12]
A.H. Qazi, F. Zallaghi, N. Torres-Acosta, et al.
Computed tomography for coronary artery calcification scoring: mammogram for the heart.
Prog Cardiovasc Dis, 58 (2016), pp. 529-536
[13]
M.J. Blaha, M.J. Budoff, A.P. DeFilippis, et al.
Associations between C-reactive protein, coronary artery calcium, and cardiovascular events: implications for the JUPITER population from MESA, a population-based cohort study.
[14]
T.S. Polonsky, R.L. McClelland, N.W. Jorgensen, et al.
Coronary artery calcium score and risk classification for coronary heart disease prediction.
JAMA, 303 (2010), pp. 1610-1616
[15]
M.J. Blaha, R.S. Blumenthal, M.J. Budoff, et al.
Understanding the utility of zero coronary calcium as a prognostic test: a Bayesian approach.
Circ Cardiovasc Qual Outcomes, 4 (2011), pp. 253-256
[16]
A. Sarwar, L.J. Shaw, M.D. Shapiro, et al.
Diagnostic and prognostic value of absence of coronary artery calcification.
JACC Cardiovasc Imaging, 2 (2009), pp. 675-688
[17]
M. Blaha, M.J. Budoff, L.J. Shaw, et al.
Absence of coronary artery calcification and all-cause mortality.
JACC Cardiovasc Imaging, 2 (2009), pp. 692-700
[18]
N.K. Kalia, L. Cespedes, G. Youssef, et al.
Motivational effects of coronary artery calcium scores on statin adherence and weight loss.
Coron Artery Dis, 26 (2015), pp. 225-230
[19]
H.S. Hecht, P. Cronin, M.J. Blaha, et al.
2016 SCCT/STR guidelines for coronary artery calcium scoring of noncontrast noncardiac chest CT scans: a report of the Society of Cardiovascular Computed Tomography and Society of Thoracic Radiology.
J Thorac Imaging, 32 (2017), pp. W54-W66
[20]
R.E. Hendrick, E.D. Pisano, A. Averbukh, et al.
Comparison of acquisition parameters and breast dose in digital mammography and screen-film mammography in the American College of Radiology Imaging Network digital mammographic imaging screening trial.
AJR Am J Roentgenol, 194 (2010), pp. 362-369
Copyright © 2023. Sociedade Portuguesa de Cardiologia
Baixar PDF
Idiomas
Revista Portuguesa de Cardiologia
Opções de artigo
Ferramentas
en pt

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos

Ao assinalar que é «Profissional de Saúde», declara conhecer e aceitar que a responsável pelo tratamento dos dados pessoais dos utilizadores da página de internet da Revista Portuguesa de Cardiologia (RPC), é esta entidade, com sede no Campo Grande, n.º 28, 13.º, 1700-093 Lisboa, com os telefones 217 970 685 e 217 817 630, fax 217 931 095 e com o endereço de correio eletrónico revista@spc.pt. Declaro para todos os fins, que assumo inteira responsabilidade pela veracidade e exatidão da afirmação aqui fornecida.