Lipid-lowering therapy and percutaneous coronary interventions

Abstract

Although technological and procedural advances have resulted in substantial improvements in clinical outcomes following percutaneous coronary interventions (PCI), recurrent coronary events may occur despite achieving optimal procedural results. Beyond myocardial revascularisation failure related to anatomical or stent-related factors, adverse cardiovascular events post PCI often arise from non-culprit lesions not treated during index interventions. While stenting treats a focal manifestation of a systemic, progressive disease, the residual risk following an acute coronary syndrome (ACS) or elective PCI is largely related to the systemic pro-atherogenic effects of suboptimally controlled cardiovascular risk factors. Lowering atherogenic lipid levels, in particular low-density lipoprotein cholesterol (LDL-C), can halt the progression of coronary atherosclerosis and improve cardiovascular outcomes to an extent that is proportional to the magnitude of LDL-C reduction. Early (in-hospital) initiation of intensive statin therapy leads to a very early clinical benefit following ACS, and prolonged adherence to optimised lipid-lowering treatment effectively reduces longer-term cardiovascular events following PCI. Therefore, achieving guideline-recommended treatment goals for LDL-C with statins and, if indicated, with the addition of non-statin lipid-lowering drugs should become a priority for all physicians involved in the treatment of patients with coronary heart disease, including comprehensive strategies initiated during the in-hospital care of patients undergoing coronary interventions. This review article summarises current evidence on the role of LDL-C in the development and progression of coronary atherosclerosis, discusses the clinical benefits of intensive lipid-lowering treatments, and presents current guideline recommendations, with emphasis on patients undergoing PCI.

Dynamic natural morphologies and component changes in nonculprit subclinical atherosclerosis in patients with acute coronary syndrome at 1-year follow-up and clinical significance at 3-year follow-up

“…Intensive LLT involves not only high doses of statins (±ezetimibe, PSCK9i, etc.) but also, more importantly, substantial LDL-C reduction based on medical therapy [18,45,46]. Even baseline LDL-C levels were not high overall in the present study, with one third of patients already on chronic statin therapy.…”

“…Vulnerable plaques are the chief culprit lesions [1][2][3][4][5][6][7][8][9], and stabilization and regression of atherosclerotic plaques are among the most important medical treatment goals for patients with acute coronary syndrome (ACS) [10][11][12][13][14]. The natural outcome of de novo coronary atherosclerotic plaques (progression or regression) is closely related to lipid-lowering therapy (LLT) not only for culprit lesions but also for nonculprit subclinical atherosclerosis [10,[15][16][17][18][19][20][21][22]. The PROS-PECT study, a natural-history study, illustrated that major adverse cardiovascular events (MACEs) during follow-up were equally attributable to recurrence at culprit and nonculprit lesion sites [23].…”

“…The PROS-PECT study, a natural-history study, illustrated that major adverse cardiovascular events (MACEs) during follow-up were equally attributable to recurrence at culprit and nonculprit lesion sites [23]. Although many studies have confirmed that aggressive LLT with high-dose statins alone or in combination with other nonstatin medical treatments leads to regression of de novo coronary plaque volume [15][16][17][18][19][20][21][22][24][25][26], some studies showed that similar lipid reduction did not result in the same degrees of plaque regression based on changes in normalized total atheroma volume (ΔTAVn) and/or percent atheroma volume (ΔPAV) measurements [24][25][26]. The underlying cause of this variation is unclear.…”

“…The development of clinical coronary intravascular imaging (IVI) technology has led to breakthroughs in the analysis of the various components of coronary plaques [27][28][29][30][31]. Due to the limitations of various IVI technological features, most studies of plaque regression or progression are conducted with intravascular ultrasound (IVUS) alone or in combination with near-infrared spectroscopy (NIRS) [15][16][17][18][19][32][33][34][35][36][37]. Although optical coherence tomography (OCT) has higher resolution, it is often unable to accurately distinguish the external elastic membrane behind the plaque due to its weak penetrating power, so the area and volume of the plaque cannot be quantified by OCT measurement; most studies of plaque outcome assessed by OCT measurement are based on changes in fibrous cap thickness or maximum lipid arc rather than plaque volume or components [38,39].…”

Clinical opportunities and healthcare impact of optimal treatment in the post-ACS patient

“…Ottimizzazione della terapia ipolipemizzante in pazienti con SCA I pazienti con SCA sono ad alto rischio di eventi ricorrenti poiché la reazione infiammatoria sistemica può determinare la crescita delle placche aterosclerotiche e la destabilizzazione di lesioni non-culprit che sono più spesso placche vulnerabili rispetto ai pazienti cronici (13). Pertanto in questi pazienti la prevenzione secondaria è fondamentale per migliorare la prognosi a breve e lungo termine.…”