Abstract
Improved prevention of cardiovascular disease (CVD) is of critical importance, as coronary heart disease (CHD) still represents the most common cause of death worldwide, engendering inestimable socioeconomic cost. The year 2015 has witnessed dramatic progress in CVD prevention on several fronts. Notably, this includes (i) event reduction in high-risk patients in general practice following introduction of a comprehensive strategy to attenuate modifiable risk factors, including lifestyle and dietary habits; (ii) the study of hybrid imaging to detect subclinical atherosclerosis, with potential improvement in risk prediction/management; (iii) the clinical demonstration, that culprit plaque rupture was observed in only 50–77% of patients with acute coronary syndromes; (iv) the emergence of ‘omics’ technologies to identify new causal biofactors; (v) the validation in clinical trials of the efficacy of monoclonal antibodies targeted to proprotein convertase subtilisin/kexin type 9 (PCSK9) in markedly reducing levels of low-density lipoprotein cholesterol (LDL-C) across a spectrum of patients at high risk of premature CVD, with preliminary findings strongly suggestive of reduction in cardiovascular events; (vi) significant reduction of cardiovascular and all-cause mortality in diabetic patients in the EMPA-REG OUTCOME trial with the anti-hyperglycaemic agent, empagliflozin, a selective sodium-glucose co-transporter-2 (SGLAT-2) inhibitor; (vii) new pharmacotherapeutic strategies for superior control of hypertension emanating from the PATHWAY-2 and PATHWAY-3 clinical trials involving spironoloactone add-on therapy in resistant hypertension, and amiloride plus hydrochlorothiazide in hypertensive patients requiring a diuretic, respectively; and finally (viii) a reduced mortality associated with a lower blood pressure target of 120 mmHg in patients at high cardiovascular risk in the SPRINT trial. Considered together, such progress augurs well for the future control of dyslipidaemia, hyperglycaemia, and hypertension, and with it, progressive reduction in atherosclerotic vascular disease and associated cardiovascular events in high-risk patients.
Highlights
The year 2015 is – and continues to be - a vintage one for seminal progress in our knowledge of the pathophysiology underlying acute coronary syndromes (ACS), and of the epidemiology, diagnosis, and prognosis of cardiovascular disease (CVD), thereby reflecting concerted efforts in our quest to prevent the global scourge of atherosclerotic vascular disease and its thrombotic complications
How can we address this insurmountable challenge? Clearly lifestyle and diet represent our first line of action as currently recommended in recent guidelines [2,3], and early identification and management of modifiable risk factors is paramount
The need for therapeutic innovation: proprotein convertase subtilisin / kexin type 9 (PCSK9) inhibition From the above, it is evident that innovative lipid lowering therapies have been - and remain urgently needed, always on a background of statin treatment whenever possible, in order to fully translate the exceptional evidence base for reduction in cardiovascular events concomitant with low-density lipoprotein cholesterol (LDL-C) lowering into reality for many dyslipidaemic patients at high risk
Summary
The year 2015 is – and continues to be - a vintage one for seminal progress in our knowledge of the pathophysiology underlying acute coronary syndromes (ACS), and of the epidemiology, diagnosis, and prognosis of CVD, thereby reflecting concerted efforts in our quest to prevent the global scourge of atherosclerotic vascular disease and its thrombotic complications. It is especially relevant that recent genetic findings, involving Mendelian randomization strategies which integrate lifelong and cumulative risk exposure, have consolidated the evidence base for a causal role of LDL in the pathophysiology of atherosclerosis and CVD [7,8,9] (Table 1).
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