A New Approach to Residual Risk in Treated Hypertension—3P Screening

Abstract

T he treatment of primary hypertension has been one of the major success stories of clinical medicine over the last 50 years. However, there is still room for further improvement because it is now appreciated that optimally treated hypertensives still have considerable residual cardiovascular (CV) risk. A recent article showed that even after correcting for systolic blood pressure (BP), a treated hypertensive patient has a 50% increased risk of any CV event.1 Intriguingly this is not the case for lipid-lowering therapy, which is able to negate all of the increased risk caused by hyperlipidemia. When the total CV risk in treated hypertension was broken down further, the increased risk of coronary disease was 46%, for stroke it was 75%, and for CV death it was 62%. Numerous other studies have found the same increased residual CV risk in treated hypertensives. 2-7 Case ReportA 65-year-old man was diagnosed with primary hypertension 15 years ago at the age of 50 years. There were no noteworthy features about this man and his family history was unremarkable. He was an ex-smoker (only 4 years) with a body mass index of 24, who ingested 10 U of alcohol per week. His hypertension was well controlled on a combination of lisinopril (20 mg) and amlodipine (5 mg). His office BPs were 130/78 mm Hg. His home BPs, recorded by himself, averaged 116/78 mm Hg. His lipid profile was normal but he was commenced on a statin 3 years ago (atorvastatin 10 mg) in view of the earlier ASCOT/LLA (Anglo Scandinavian Cardiac Outcomes Trial/Lipid Lowering Arm) study results.Despite the above, he was admitted to hospital with an anterior ST-segment-elevation myocardial infarction (STEMI), which was appropriately treated with angioplasty and all other routine therapy, including the addition in the long term of aspirin, a β-blocker, and an increase in atorvastatin dose (to 80 mg). His most recent investigation showed a reduced left ventricular (LV) ejection fraction of 42%.Having been told that his BP was well controlled, he was puzzled as to why he had developed an overt CV event (an STEMI) which now put him at risk of future heart failure and why his physicians had not been able to either better predict the STEMI or better still prevent it occurring. His case illustrates well residual risk in treated hypertension. Residual Risk in Treated HypertensionA knee-jerk response to improve the situation with regard to residual risk in hypertension would be to target a lower achieved BP than is currently advised. However, attempts to do this have generally disappointed (ie, efforts to achieve a lower than current target BP have not delivered extra benefit and adverse effects have been prominent). 8 We obviously need a smarter approach to this problem. 9To address residual risk, the first question we need to ask is what (silent) CV abnormalities are actually present in optimally treated hypertensives that may be causing the residual risk. Nadir et al 10 recently showed that 34% of optimally treated hypertensives have silent, asymptomatic cardiac abnorma...

A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage

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Inflammatory cytokines regulate renal sodium transporters: how, where, and why?

“…Renal and vascular dysfunction are important causes and consequences of this disease and lead to the development of heart failure, stroke, myocardial infarction, and chronic kidney disease, resulting in substantial morbidity and mortality (16,32). Alarmingly,~50% of patients with hypertension have uncontrolled blood pressures, and, even when blood pressures are reasonably controlled, these patients have an elevated risk of cardiovascular disease (3,21,29). Unfortunately, we do not fully understand the pathophysiology of essential hypertension, but alterations in renal sodium transport appear to be a final common pathway in most forms of this disease as discussed below.…”

The Value of N-Terminal Pro–B-Type Natriuretic Peptide in Determining Antihypertensive Benefit

“…Whether cardiac biomarkers can help phenotype and apply a stratified medicine approach to treating patients with hypertension optimally remains to be seen. 21 It is of note that lowering of NT-proBNP in patients with HF is an established marker of improved outcome. 22 Therefore, it is plausible that more subtle absolute treatment-associated changes in NT-proBNP in individuals without HF (ie, primary prevention populations) may also predict benefit.…”