Guideline for the diagnosis and management of hypertension in adults — 2016

We thank Rodgers and colleagues for their comments regarding our article.1 We debated dropping the term “hypertension”, an arbitrary construct indeed, from the guideline but concluded that we would communicate more effectively with our target audience (practising clinicians in primary care) by retaining this widely used term.

The full guideline summarised in our article recommends broad adoption of healthy lifestyle measures (https://www.heartfoundation.org.au/images/uploads/publications/PRO-167_Hypertension-guideline-2016_WEB.pdf). The lifestyle section begins: “Lifestyle advice is recommended for all patients with or without hypertension and regardless of drug therapy”. Importantly, a healthy lifestyle confers additional benefits (eg, biomechanical) over a pharmacologically based risk reduction approach.

The quote on combination therapy is taken out of context from a listing of possible arguments for and against initiating treatment with a fixed dose combination. The guideline statement is fair and balanced when read in context, and is supported by the references provided by Rodgers and colleagues. These articles comparing monotherapy and combination therapy address the effects on blood pressure (BP) per se, not cardiovascular outcomes.

Our guideline advises consideration of cardiovascular risk in making treatment decisions. However, we are not convinced that the National Vascular Disease Prevention Alliance Guidelines for the management of absolute cardiovascular disease risk (http://www.cvdcheck.org.au/pdf/Absolute_CVD_Risk_Full_Guidelines.pdf) provides safe guidance for management of hypertension. That guideline permits leaving BP untreated up to 180/110 mmHg. Early BP trials showed substantial benefit and reduction in serious injury from treating patients with hospital diastolic BP averaging 107 mmHg compared with untreated controls (number needed to treat, 3.8).2

Conversely, analyses suggesting benefit from lowering BP in normotensive patients rely almost entirely on studies in heart failure, myocardial infarction or both.3 In these studies, treatment was aimed at blocking the sympathetic and renin–angiotensin systems. BP lowering was regarded as a treatment-limiting adverse effect (eg, “patients were excluded if they had a systolic blood pressure lower than 85 mmHg”4). In these settings, calcium channel blockade also lowered BP but, importantly, did not provide benefit.5

Evidence from clinical trials in specific populations such as patients with heart failure or myocardial infarction cannot sensibly be used to support lowering BP in, say, normotensive smokers with high cholesterol. In such individuals, smoking cessation and a statin are more beneficial.6

We favour a nuanced approach to treatment of both hypertension and cardiovascular risk over a Procrustean one. We are confident that clinicians are up to the task.