European Journal of Cardiovascular Medicine

Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death and disability worldwide, despite significant advances in preventive cardiology and lipid-lowering therapies [1]. Central to ASCVD risk reduction is the management of low-density lipoprotein cholesterol (LDL-C), which has long been established as a primary therapeutic target.[1] Robust clinical evidence demonstrates that lowering LDL-C significantly reduces cardiovascular events, and international guidelines consistently recommend aggressive LDL-C control for high-risk individuals [1,7].

In addition to LDL-C,. Lipoprotein(a) [Lp(a)] has emerged as a genetically determined, independent risk factor that confers additional cardiovascular risk—even among patients with optimally managed LDL-C [2,3].

Elevated lipoprotein(a) [Lp(a)] levels, defined as >50 mg/dL, are present in approximately one in five individuals globally and are associated with enhanced atherogenesis, inflammation, and thrombosis. The prevalence is notably higher among South Asians, affecting roughly 25% of individuals, compared with Western populations.(4,18)

Despite the well-established roles of LDL-C and Lp(a) in ASCVD pathogenesis, there remains a significant gap in clinical practice. Many healthcare professionals are either unaware of the importance of Lp(a) or do not routinely incorporate its measurement into cardiovascular risk assessment [5,6]. Similarly, while LDL-C management is widely acknowledged, real-world practice often falls short of guideline-recommended targets, and the interplay between LDL-C and Lp(a) is frequently overlooked [3].

To better understand these gaps, we conducted a survey on healthcare professionals at the CSI Congress. The aim was to assess current awareness, perceptions, and treatment practices related to LDL-C and Lp(a) in the context of ASCVD. The insights gained from this survey will help us identify the need gap in understanding among healthcare professionals regarding LDL-C and Lp(a).

Aims and Objectives

The primary aim of this survey was to evaluate healthcare professionals’ awareness, understanding, and clinical practices related to LDL C and Lp(a) management in the context of ASCVD.

An anonymised, structured, closed‑ended questionnaire was developed to evaluate healthcare professionals’ awareness, perceptions, and clinical practices regarding LDL‑C and lipoprotein(a) management in ASCVD. Prepared and reviewed by the NVS medical team, the survey was designed to capture key aspects of lipid management, including clinician specialty, and routine practice behaviours. Additional questions assessed approaches to ASCVD risk stratification, LDL‑C target selection, preferred treatment strategies for patients not achieving lipid goals, and the use and interpretation of Lp(a) testing. Items also explored thresholds for treatment escalation—particularly the adoption of injectable lipid‑lowering therapies—and perceived barriers to incorporating Lp(a) measurement into routine care. The survey was conducted during the Cardiological Society of India (CSI) Congress 2025, held in Delhi from 4th to 7th December, leveraging the large gathering of cardiologists and cardio‑physicians attending the conference. Approximately 2,500 delegates participated in the congress, of whom around 400 healthcare professionals voluntarily visited the Novartis medical booth. Survey participation was based on voluntary engagement at the booth, resulting in a self‑selected cohort of respondents. All healthcare professionals visiting the Novartis‑sponsored medical booth were eligible to participate. Respondents completed the digital survey via Microsoft Forms using a QR code displayed at the booth. Participation was voluntary, with no incentives provided. All study materials were reviewed and approved by an external independent ethics committee (IEC‑SNH; ECR/1148/Inst/DL/2018/RR‑21). Responses were compiled and analysed descriptively, with results presented in aggregate to identify trends and gaps in clinical practice.

Respondents

A total of 201 clinicians completed the survey. Most were cardiologists (n=167; 83%), followed by internal-medicine practitioners involved in cardiology (n=21), general medicine practitioners (n=7), cardiothoracic surgeons (n=2), and others (n=4)

ASCVD risk classification

When classifying patients with a recent cardiovascular event, 64% categorized them as high risk and 20% as very high risk.  For stable ASCVD with an event 20 years ago, 72% considered them moderate risk and 11% very high risk. (Figure 1)

LDL-C targets
Among all respondents, 55.7% aimed for an LDL‑C target of <70 mg/dL, 20.4% targeted <55 mg/dL, and 12.9% aimed for <55 mg/dL and/or ≥50% reduction from baseline. The remaining participants followed either a ≥50% reduction-only target or a <100 mg/dL target.

Follow-up LDL-C testing

First follow-up LDL-C testing was most commonly aimed at 6 weeks (60%), followed by within 4 weeks (32%). Figure 3 – Timing of first follow-up LDL-C test

Use and thresholds for injectable lipid-lowering therapy

Use of injectable lipid-lowering therapies was low, with 77% reporting <10% of patients on injectables. Injectable therapy was usually considered at LDL-C ≥150 mg/dL (59%), while only 6% used the recommended cut-off of ≥135 mg/dL.

Figure 4 – (A) Share of patients on injectables; (B) LDL‑C thresholds to initiate injectables

Next-step therapy when statin monotherapy is insufficient

When very high‑risk patients did not achieve LDL‑C targets on statin monotherapy, clinicians most commonly preferred statin plus ezetimibe (n=158; 78.6%), followed by statin plus ezetimibe + PCSK9 inhibitor which includes either Inclisiran or monoclonal antibodies (n=14; 7.0%), statin plus PCSK9 monoclonal antibodies (n=12; 6.0%), statin plus bempedoic acid (n=7; 3.5%), statin plus inclisiran (n=5; 2.5%), and statin plus bempedoic acid + PCSK9 inhibitor which includes either Inclisiran or monoclonal antibodies  (n=5; 2.5%).

Lipoprotein(a): awareness, testing, thresholds, and barriers

Awareness and practice patterns related to Lipoprotein(a) were assessed based on self‑reported responses from participating clinicians. Overall, 65% reported understanding the role of Lp(a) but routine testing was uncommon (17% routinely, 35% occasionally). Testing was mainly for premature ASCVD or family history (59%), suspected familial hypercholesterolemia (33%), and intermediate risk (28%). The threshold for elevated Lp(a) was most commonly  considered as ≥70 mg/dL (44%), followed by ≥50 mg/dL (32%). When Lp(a) was high, 43% advised lifestyle changes, 41% intensified lipid therapy, and 13% took no action. Over half were unaware of its higher atherogenicity compared to LDL-C. Barriers to testing included cost, lack of awareness, absence from standard panels, and no targeted therapy.

Figure 5 – Lp(a) panels (familiarity, testing, who to test, barriers)

This survey, conducted among clinicians predominantly from cardiology, highlights persistent gaps between guideline recommendations and real-world practice in lipid management. Despite clear guidance from the European Society of Cardiology/European Atherosclerosis Society (ESC/EAS, 2019), Cardiological Society of India (CSI, 2024), and Lipid Association of India (LAI, 2023), risk stratification and LDL-C target adoption remain suboptimal. All patients with documented ASCVD—including those with prior myocardial infarction, stroke, or peripheral arterial disease—should be classified as “very high risk” for future cardiovascular events, irrespective of time since the last event. These guidelines emphasize that risk does not revert to “moderate” or “high” simply due to the passage of time but is determined by the presence of clinical ASCVD and associated risk enhancers [1,7,8]. This principle is particularly relevant in India, where premature and recurrent ASCVD burden is high, underscoring the need for aggressive risk factor modification.

Guidelines recommend an LDL-C goal of <55 mg/dL and ≥50% reduction from baseline for very high-risk patients [1,7,8]. However, most clinicians continue to aim for <70 mg/dL, reflecting a significant need gap. Evidence from landmark trials reinforces the importance of intensive LDL-C lowering: in FOURIER OLE, cardiovascular event incidence was approximately 32% higher in individuals with LDL-C ≥70 mg/dL compared to those with <55 mg/dL [9], while IMPROVE-IT demonstrated a 2% absolute risk reduction with more aggressive LDL-C lowering [10]. Meta-analyses further confirm that each 1 mmol/L LDL-C reduction lowers major coronary events by 24%, and every 10 mg/dL increase raises the odds of multi-site atherosclerosis by 18% [11]. These findings validate the principle that “lower is better” and highlight the importance of achieving guideline-recommended targets.

Real-world practice reveals delays in therapy escalation. The conventional stepwise approach—statin, then ezetimibe, then PCSK9 inhibitor or inclisiran—often postpones achieving LDL-C goals, leaving patients vulnerable during the high-risk post-discharge period when up to 50% of recurrent events occur within 90 days [17]. Less than 40% of patients achieve LDL-C <55 mg/dL with this approach, and Indian data show only 21% reach this target at one year [13–15]. Recent expert consensus advocates a simplified two-step strategy: initiate high-intensity statin plus ezetimibe, and add a PCSK9 inhibitor or inclisiran if LDL-C <55 mg/dL is not achieved within 4–8 weeks [13,16]. Early and intensive combination therapy triples the likelihood of achieving LDL-C targets and reduces major adverse cardiovascular events compared to traditional escalation [13].

While LDL-C remains the cornerstone of lipid management, another critical and often overlooked risk factor is Lipoprotein(a) [Lp(a)]. Structurally, Lp(a) consists of an LDL-like particle covalently bound to apolipoprotein(a), imparting additional atherogenic and prothrombotic properties. It is approximately six times more atherogenic than LDL on a per-particle basis, and elevated levels (≥125 nmol/L or 50 mg/dL) occur in about 20% of individuals [1,4]. Unlike LDL-C, Lp(a) levels are genetically determined, remain stable throughout life, and are unaffected by diet or environmental factors. Elevated Lp(a) confers a 1.5-fold increased risk of cardiovascular mortality and is considered a monogenic, causal risk driver of ASCVD [1,7].

Guidelines from ESC/EAS and CSI recommend at least one-time measurement of Lp(a) in all adults, particularly those with premature ASCVD, familial hypercholesterolemia, or intermediate/uncertain risk profiles [1,7]. The threshold for elevated Lp(a) is ≥50 mg/dL (or ≥125 nmol/L), above which cardiovascular risk rises significantly. Despite these recommendations, routine testing remains uncommon, largely due to limited awareness, cost, lack of inclusion in standard lipid panels, and absence of targeted therapies.

Current practice shows variability in defining elevated Lp(a) and uncertainty regarding management. While some clinicians intensify lipid-lowering therapy or provide lifestyle counseling when Lp(a) is high, others take no specific action. Knowledge gaps persist, with many clinicians unaware of Lp(a)’s relative atherogenicity compared to LDL-C. Barriers to routine testing—such as cost, lack of awareness, and absence from standard panels—underscore the need for broader education and system-level changes. Incorporating Lp(a) into standard risk assessment and leveraging emerging therapies will be critical to improving cardiovascular prevention strategies.

Limitations

This survey was conducted at a single national cardiology scientific conference and included healthcare professionals who voluntarily participated by visiting a Novartis medical booth. As such, the study population may reflect clinicians with a greater baseline interest or familiarity with lipid disorders, which could introduce selection bias. Responses were self reported and based on participants’ understanding and recall rather than objective clinical data, introducing the potential for recall bias. In addition, the use of predefined response options and the absence of explicit definitions for certain terms (for example, “recent” events) may have limited the granularity of responses and led to variability in interpretation. The inclusion of clinicians both with and without prior interaction with the field team may also have introduced heterogeneity in baseline exposure. Collectively, these factors should be considered when interpreting the findings and may limit generalizability to the broader cardiology or specialist community. Nonetheless, the results highlight important practice relevant gaps and underscore the need for more comprehensive real world data generation to better understand unmet clinical needs, while also identifying an opportunity to improve awareness and adoption of recommended LDL C targets in routine practice.

This survey underscores significant gaps in lipid management among clinicians, despite strong guideline recommendations. Risk stratification for ASCVD remains inconsistent, and LDL-C targets for very high-risk patients are often less aggressive than recommended. The delays in therapy intensification and underutilization of combination therapy still persist. Similarly, awareness and routine testing for Lipoprotein(a) [Lp(a)]—a recognized, independent risk enhancer—remain limited due to cost, lack of inclusion in standard panels, and absence of targeted therapies. Addressing these gaps through clinician education, system-level changes, and early adoption of guideline-based strategies, including intensive LDL-C lowering and Lp(a) assessment, is essential to optimize secondary prevention and reduce the burden of recurrent cardiovascular events. Funding Sources: This survey was funded by Novartis. No honoraria, incentives, or financial support were provided to participating respondents

1.      Mach F, Baigent C, Catapano AL, Koskinas KC, Casula M, Badimon L, et al. 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J. 2020;41(1):111–188.

2.      Kronenberg F. Human genetics and the causal role of lipoprotein(a) for various diseases. Cardiovasc Res. 2021;117(1):33–53.

3.      Bhatia HS, Wandel S, Willeit P, Gencer B, Tsimikas S, Mach F, et al. Independence of lipoprotein(a) and low-density lipoprotein cholesterol–mediated cardiovascular risk: a participant-level meta-analysis. Circulation. 2025;151(4):312–321.

4.      Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, et al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010;31(23):2844–2853.

5.      Cruz-Bautista I, Flores-Jurado Y, Roa-Álvarez G, Aguilar-Salinas CA, et al. Lipoprotein(a) levels and clinical decision-making: data from a Mexican cohort at a tertiary medical institution. Lipids Health Dis. 2025;24(1):192.

6.      Loh WJ, Watts GF, Lum E. A short educational video for improving awareness and confidence of healthcare professionals in managing lipoprotein(a): a pilot study based on LILAC-for-Lp(a). Eur J Cardiovasc Nurs. 2025 Mar 28:zvaf052.

7.      Sawhney JP, Ramakrishnan S, Madan K, Kaul U, Singhal A, Mohan JC, et al. CSI clinical practice guidelines for dyslipidemia management: executive summary. Indian Heart J. 2024;76(Suppl 1):S6–S19.

8.      Puri R, Bansal M, Mehta V, Iyengar SS, Narasingan SN, Duell PB, et al. Lipid Association of India 2023 update on cardiovascular risk assessment and lipid management in Indian patients: consensus statement IV. J Clin Lipidol. 2024;18:e351–e373.

9.      Fernández-Friera L, Peñalvo JL, Fernández-Ortiz A, Ibañez B, López-Melgar B, Laclaustra M, et al. Normal LDL-cholesterol levels are associated with subclinical atherosclerosis in the absence of risk factors. J Am Coll Cardiol. 2017;70(24):2979–2991.

10.   Patel PN, Giugliano RP. Targeting LDL cholesterol in the secondary prevention of atherosclerotic cardiovascular disease. Glob Cardiol Sci Pract. 2020;2020(3):e202039.

11.   Gaba P, O'Donoghue ML, Park JG, Wiviott SD, Atar D, Kuder JF, et al. Association between achieved low-density lipoprotein cholesterol levels and long-term cardiovascular and safety outcomes: an analysis of FOURIER-OLE. Circulation. 2023;147(16):1192–1203.

12.   Ray KK, Haq I, Bilitou A, Manu MC, Burden A, Aguiar C, et al. Treatment gaps in the implementation of LDL cholesterol control among high- and very high-risk patients in Europe between 2020 and 2021: the multinational observational SANTORINI study. Lancet Reg Health Eur. 2023;29:100624.

13.   Patti G, Spinoni EG, Mennuni M, Mehran R, Fabrizio F, Ferlini M, et al. Safety and efficacy of very low LDL-cholesterol intensive lowering: a meta-analysis and meta-regression of randomized trials. Eur Heart J Cardiovasc Pharmacother. 2025;11(2):143–154.

14.   Jain M, Sawant R, Panchal H, Anand S, Jena A, Gupta R, et al. Evaluating LDL-C control in Indian acute coronary syndrome (ACS) patients – a retrospective real-world study. Int J Cardiol Cardiovasc Risk Prev. 2023;19:200210.

15.   Bansal M, Kasliwal RR, Chandra P, Kapoor R, Chouhan N, Bhan A, et al. Attainment of low-density lipoprotein cholesterol goals in patients undergoing coronary revascularization in the contemporary clinical practice. Indian Heart J. 2024;76(6):414–417.

16.   Rao SV, O'Donoghue ML, Bhatt DL, Boden WE, Cannon CP, de Lemos JA, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2025;151(13):e771–e862.

17.   Nedkoff L, Briffa TG, Knuiman M, Hung J, Sanfilippo FM. Short-term recurrence and mortality after a first myocardial infarction: a population-level study. Int J Cardiol Cardiovasc Risk Prev. 2023;17:200185

18.  Patel D, Koschinsky ML, Agarwala A, Natarajan P, Bhatia HS, Mehta A, Patel J, Peters M, Pandya S, Sagheer U, Puri R. Role of lipoprotein (a) in atherosclerotic cardiovascular disease in South Asian individuals. Journal of the American Heart Association. 2025 Jul 15;14(14):eJAHA-2024.