Shooting beyond score

Abstract

ypertension is a complex disease, in whichelevated blood pressure reflects the impairmentof several regulatory and contraregulatory mech-anisms and systems. This, in turn, may lead to developmentandprogressionofasymptomaticsubclinicalorgandamage,hence promoting cardiovascular and renal diseases.During the long natural history of hypertensive disease,the presence of hypertension-related organ damage atcardiac, vascular and renal level has been demonstratedto largely and substantially impact prognosis in terms ofincreased incidence of cardiovascular and renal outcomesin large clinical trials. In turn, evidence derived from rela-tively smaller clinical studies or predefined analyses fromrandomized clinical trials have demonstrated that preven-tion, delayed progression or even regression of organdamageduringchronicantihypertensivetherapymaytrans-late into significant cardiovascular benefits.A paradigmatic example, is provided by the LosartanInterventionForEndpointreductioninhypertensiontrialinwhichthepresenceofleftventricularhypertrophy(LVH)ormicroalbuminuria(MAU)orbothatbaselinewasassociatedwith a significant increased risk of developing the primarycomposite endpoint (myocardial infarction, stroke andcardiovascular mortality) and mostly stroke during thefollow-up [1,2]. This increased risk was also largely inde-pendentofhoworgandamagewasassessed(electrocardio-graphic-LVH criteria with or without ST-segment strain orechocardiographic criteria for LVH) and it was not strictlyrelated to the concomitant treatments or blood pressurechanges during the study. In the same study, regression ofLVH [3,4] or MAU [5] was paralleled by a progressive,persistent and significant reduction of the risk ofcardiovascular outcomes. Other studies have linkedregression of LVH to cardiovascular benefits in hyperten-sion [6–9].Giventheimportanceofthepresenceand,mostly,ofthedevelopment of hypertension-related organ damage in theclinicalmanagementofhypertension, itisquitedisappoint-ing that no major attempt has yet been made to considermarkers of hypertension-related organ damage in moderntools and charts for cardiovascular risk assessment andevaluation developed and adopted in the US (FraminghamScore) or European [10] countries. The only risk algorithmthat has systematically taken into consideration the pres-ence/absence of organ damage in the definition of esti-mated added cardiovascular risk is represented by theEuropean Society of Hypertension/European Society ofCardiology (ESH/ESC) guidelines [11,12].Inclusion of markers of organ damage to risk charts orcalculators is feasible and can be done at low cost, especi-ally when the least expensive parameters (electrocardio-graphic-LVH, MAU, estimatedglomerular filtrationrate)areused. This may translate in improved cardiovascular riskstratification and more precise prognosis especially inintermediate-to-high risk patients. So, it is probably timeto take advantage from this and focus more on theseintermediate disease markers in risk charts applied tohypertensives.In this latter regard, Sehestedt et al. [13] in a previousstudy were able to demonstrate that in an apparentlyhealthy population, subclinical organ damages, as well asthe number of abnormal parameters indicating subclinicalorgan damage, were associated with increased cardiovas-cular risk, independently of Systematic COronary RiskEvaluation (SCORE). Combining the risk models of SCOREand subclinical organ damage yielded greater performanceon risk stratification and derived recommendations forprimary prevention. This approach allows reclassificationof the cardiovascular risk as defined by SCORE by simplyadding LVH and MAU. For example, in patients with aSCORE of 5% or more, the cardiovascular risk would bedoubled when taking into account the presence of any ofthese two markers of organ damage. At the same time, inpatients with a SCORE less than 5%, the presence of LVHalmost doubles the cardiovascular risk, whereas thepresence of MAU increases cardiovascular risk by morethan three-fold compared with those without MAU. Thiswas consistent with former Italian studies showing thatidentification of subclinical organ damage reclassify therisk profile of hypertensive patients [14].Anewanalysisperformedbythesamegroup[15],whichis published in this issue of the Journal, assessed the