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News briefs

Unnecessary EOL treatment widespread

University of New South Wales reviewers, reporting in the International Journal for Quality in Health Care, have found that more than a third of elderly patients hospitalised at the end of their life received “invasive and potentially harmful medical treatments”. The analysis of 38 studies over 2 decades, based on data from 1.2 million patients, bereaved relatives and clinicians in 10 countries including Australia, found that the practice of doctors initiating excessive medical or surgical treatment on elderly patients in the last 6 months of their life continues in hospitals worldwide. Dr Magnolia Cardona-Morrell, who led the research at UNSW’s Simpson Centre for Health Services Research, said rapid advances in medical technology have fuelled unrealistic community expectations of the healing power of hospital doctors and their ability to ensure patients’ survival. “It is not unusual for family members to refuse to accept the fact that their loved one is naturally dying of old age and its associated complications and so they pressure doctors to attempt heroic interventions,” Dr Cardona-Morrell said. “Doctors also struggle with the uncertainty of the duration of the dying trajectory and are torn by the ethical dilemma of delivering what they were trained to do, save lives, versus respecting the patient’s right to die with dignity.” The study revealed 33% of elderly patients with advanced, irreversible chronic conditions were given non-beneficial interventions such as admission to intensive care or chemotherapy in the last two weeks of life while others who had not-for-resuscitation orders were still given CPR. The researchers also found evidence of invasive procedures, unnecessary imaging and blood tests, intensive cardiac monitoring and concurrent treatment of other multiple acute conditions with complex medications that made little or no difference to the outcome, but which could prevent a comfortable death for patients.

Breast cancer treatment impacts independent living

Researchers from the US have found one in five women undergoing breast cancer treatment for a year became “incapable of performing some of the basic tasks required for independent living”. Published in Cancer, the study also found that a simple survey can help identify which women are at risk of such functional decline. Cynthia Owusu from Case Western Reserve University in Cleveland, Ohio, and her colleagues studied a group of 184 women aged 65 years and older who had been recently diagnosed with stage I to III breast cancer. The researchers used the Vulnerable Elders Survey, a 13-item self-administered tool that has been validated in community-dwelling elders to predict functional decline or death within 12 months. Patients completed the survey just prior to breast cancer treatment. Within 12 months, 34 of the 184 patients developed functional decline and seven died. The risk of functional decline or death rose with increasing survey scores. Women without an education beyond high school were disproportionately affected. “Our findings are important because the study validates the Vulnerable Elders Survey as a useful tool for identifying older women with breast cancer who may be at increased risk for functional decline within a year of treatment initiation,” she said. “This instrument offers the opportunity for early identification and will inform the development of interventions to prevent and address functional decline for those particularly at risk, such as women with low socioeconomic status.”

Appropriate use of serum troponin testing in general practice: a narrative review

In this article, we review the evidence regarding troponin testing in a community setting, particularly relating to new information on the utility of high sensitivity assays and within the context of contemporary guidelines for the management of chest pain and the acute coronary syndrome. For this review, we synthesised relevant evidence from PubMed-listed articles published between 1996 and 2016 and our own experience to formulate an evidence-based overview of the appropriate use of cardiac troponin assays in clinical practice. We included original research studies, focusing on high quality randomised controlled trials and prospective studies where possible, systematic and other review articles, meta-analyses, expert consensus documents and specialist society guidelines, such as those from the National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand. This article reflects our understanding of current state-of-the-art knowledge in this area.

What is the purpose of the serum troponin assay?

The troponin assay was designed to assist in diagnosis and improve risk stratification for people presenting in the emergency setting with symptoms suggestive of an acute coronary syndrome.1,2 These symptoms include:

  • chest, jaw, arm, upper back or epigastric pain or pressure

  • nausea

  • vomiting

  • dyspnoea

  • diaphoresis

  • sudden unexplained fatigue.

As the troponin assay was not designed for use in clinical contexts outside that of a possible acute coronary syndrome, an elevated troponin level in a patient without this history, although of prognostic value, is not likely to be due to myocardial infarction unless it was caused by a clinically silent event. The troponin test result should always be interpreted with reference to symptoms, comorbidities, physical examination findings and the electrocardiogram (ECG). The degree of troponin elevation is also used for quantifying the size of myocardial infarction, although it is not well validated for this purpose.3,4

What are the causes of serum troponin elevation?

Unlike the earlier creatine kinase assay, which was not specific to cardiac muscle, troponins are structural proteins unique to cardiac myocytes, and any elevation represents cardiac muscle injury or necrosis. Most cardiac troponin is attached to the myofilaments, but about 5% is free in the cytosol. In acute myocardial infarction or following cardiac trauma, there is disruption of the sarcolemmal membrane of the cardiomyocyte and release of the troponin in the cytoplasmic pool. There is a delay in the appearance of troponin in serum of between 90 and 180 minutes,57 which means there is a requirement for serial testing of troponin levels in hospital emergency departments. Later, there is a prolonged release of troponin from the degradation of myofilaments over 10–14 days.

It is now clear that troponin may also be released under conditions of myocardial stress without cellular necrosis (including tachyarrhythmia, prolonged exercise, sepsis, hypotension or hypertensive crisis and pulmonary embolism)8,9 (Box 1), probably through the mechanism of stress-induced myocyte bleb formation10 and release of a small portion of the cytoplasmic troponin pool. Elevations of troponin seen in this context are sometimes erroneously referred to as “false positives”; this is incorrect because any troponin elevation is truly abnormal and is prognostic in many clinical states outside of the acute coronary syndrome.11

The serum troponin assay was designed to screen patients for spontaneous, usually atherothrombotic, myocardial infarction, but under the new classification of myocardial infarction (Box 2),12 troponin elevations associated with demand–supply imbalance have led to the new diagnostic category of type 2 myocardial infarction (which is more likely to be associated with reversible or minimal myocardial injury, rather than permanent myocardial necrosis). The prevalence of all types of myocardial infarction, particularly type 2, has been amplified by the new high sensitivity troponin assays. A rise and fall in serum troponin level is required to confirm an acute myocardial infarction, irrespective of the type of troponin assay used. Chronic stable elevations are seen in some conditions (eg, chronic heart failure) where the lack of change over time indicates that an acute process is not present. True instances of false-positive troponin elevation due to calibration errors, heterophile antibodies or interfering substances have been greatly reduced by improved analytical techniques, blocking reagents and the use of antibody fragments.

What is different about the new high sensitivity troponin assays?

The newly developed high sensitivity assays provide reliable detection of very low concentrations of troponin and therefore offer earlier risk stratification of patients with possible acute coronary syndrome (3 hours after an episode of chest pain).7 The high sensitivity assays are also presented in different units (ng/L, rather than the previous μg/L), enabling the reporting of whole numbers (eg, 40 ng/L is equivalent to the earlier assay report of 0.04 μg/L).

By expert consensus, the assay must have a coefficient of variance of < 10% at the 99th percentile value of a reference population,13 which is the cut-off used for elevation. The benefit of the improved precision of the new high sensitivity assays is that even small elevations above this cut-off can be considered a true elevation, rather than an artefact of the assay. Examples of cut-off for elevation (> 99th percentile of a reference population) include a high sensitivity troponin T (hsTnT; Roche Elecsys) level of 14 ng/L, and a high sensitivity troponin I (hsTnI; Abbott Architect) level of 26 ng/L (these values may differ between pathology laboratories). It has been suggested that sex-specific cut-off values should be provided,12 and, in Australia, laboratories reporting the hsTnI assay often use these differing cut-offs (female, 16 ng/L; male, 26 ng/L).

A study in an Australian hospital found that use of the high sensitivity assays was associated with significantly earlier diagnosis and less time spent in the emergency department, but did not change the revascularisation rate or reduce mortality.14 A recent meta-analysis demonstrated that about 5% of an asymptomatic community population had an elevated serum troponin level when tested using a high sensitivity assay,11 clearly different to the reference population (screened to exclude comorbidities) that was used to derive the assay cut-off. Even in this asymptomatic cohort, an elevated troponin level had prognostic significance and was associated with a threefold greater risk of adverse cardiac outcomes compared with people with normal troponin levels. This reflects a greater hazard than identified previously for those with elevated cholesterol (risk ratio [RR], 1.9) or diabetes, (RR, 1.7) or even from smoking (RR, 1.68).15

As older patients (aged ≥ 65 years) have a high prevalence of elevated troponin levels, a higher troponin cut-off has been proposed for this group.16,17 More than 50% of patients with heart failure have elevated high sensitivity troponin levels, and the level is correlated with prognosis.18 It has also been shown in a large cohort of patients with chronic atrial fibrillation who were taking anticoagulant therapy19 that troponin elevation was independently related to the long term risk of cardiovascular events and cardiac death.

When should a general practitioner measure serum troponin and what should be done if a high serum troponin level is found?

Patients who present with a history of a possible acute coronary syndrome, but have been symptom-free for between 24 hours and 14 days previously, and who have no high risk features (ongoing or recurrent pain, syncope, heart failure, abnormal ECG) could be assessed with a single serum troponin test. If patients have had ongoing symptoms within the preceding 24 hours, they should be referred immediately to an emergency department for assessment.20 For patients in whom a single troponin test is appropriate, the test should be labelled as urgent and, as the result has prognostic implications and may require an urgent action plan, a system must be in place to ensure medical notification of the result at any hour of the day or night. In this clinical context, even a small elevation in serum troponin level may indicate an acute coronary syndrome during the preceding 2 weeks, warranting urgent cardiac assessment and hospital referral.20 However, a negative serum troponin result in the absence of high risk features does not exclude a diagnosis of unstable angina, and urgent cardiac assessment would still be appropriate if the presenting symptoms are severe or repetitive.

When should a general practitioner not measure serum troponin?

Patients presenting with a possible acute coronary syndrome with symptoms occurring within the preceding 24 hours, or with possible acute coronary syndrome more than 24 hours previously and with high risk features such as heart failure, syncope or an abnormal ECG, require further investigations.20 These may include urgent angiography, serial troponin testing and further ECGs in a monitored environment where emergency reperfusion treatments are available. These patients should be referred and transported to a hospital emergency department by ambulance, as it is not appropriate to perform serial troponin testing of high risk patients in a community setting.20 High risk ECG abnormalities include tachyarrhythmia or bradyarrhythmia, any ST deviation, deep T wave inversion or left bundle branch block. Serial troponin testing is required to confirm a diagnosis of myocardial infarction, and these patients may require fibrinolysis or urgent angiography and revascularisation.

Measurement of troponin in asymptomatic people is not currently recommended as the result may be problematic, with multiple possible causes and no clearly effective investigative strategies or therapies, and has to be interpreted with respect to the entire clinical context.

Case reports of appropriate and inappropriate use of troponin testing

Patient 1

A 72-year-old woman with type 2 diabetes tells you that she had 2 hours of chest tightness 4 days ago, but has been feeling well since then. Her physical examination is unremarkable, and you think her ECG is normal. You arrange for her to have an urgent serum troponin test, and the result is significantly elevated (hsTnI, 460 ng/L; female reference interval [RI], < 16 ng/L). You call a cardiologist, who arranges her immediate admission to hospital. Echocardiography shows hypokinesis of the anterior wall and apex and a left ventricular ejection fraction of 48%. Angiography shows a severe proximal left anterior descending artery lesion, which is treated with coronary stenting, and minor disease of the other arteries. She is discharged and has a good outcome.

Comment

In this setting, measurement of troponin is reasonable, as her symptoms occurred 4 days previously and she has had no further symptoms and has no high risk features.

Patient 2

A 68-year-old man presents to your surgery with a history of severe chest tightness lasting for 2 hours that morning. It has now resolved and he is pain-free 5 hours later. He has no major cardiovascular risk factors and his physical examination and ECG are normal. You do not order any other tests and arrange ambulance transport to a hospital emergency department. Testing at the hospital shows that his hsTnI level is elevated (84 ng/L; male RI, < 26 ng/L), and angiography shows severe left main coronary artery disease. He undergoes coronary revascularisation and has a good outcome.

Comment

This patient has had possible acute ischaemic symptoms within the past 24 hours. Troponin testing in a general practice setting should therefore not be performed, and the actions taken in sending this patient for urgent assessment are appropriate.

Patient 3

A 62-year-old man with no relevant past medical history presents with a history of several episodes in the past week of dull central chest pain lasting 5–10 minutes; the latest episode was 3 days ago. His physical examination and ECG are considered normal. An urgent serum troponin assay is performed and the result is normal (hsTnI, 3 ng/L; male RI, < 26 ng/L). You are worried that his clinical presentation may still be consistent with unstable angina. You contact a cardiologist, who arranges a stress echocardiogram the following day, which is strongly positive. The patient is admitted and is found to have severe three-vessel coronary artery disease. He undergoes revascularisation, with a good outcome.

Comment

This patient presents with symptoms suggestive of unstable angina. In this setting, irrespective of any troponin values, further urgent assessment is required.

Patient 4

A 52-year-old obese man with controlled hypertension has had multiple episodes in the past 12 months of prolonged retrosternal burning pain. These have often lasted several hours and are particularly worse after meals and when recumbent. He has had no symptoms for the past 4 days. His physical examination and ECG are normal. A serum troponin test result is normal. You arrange a stress echocardiogram, which is normal, and an upper gastrointestinal endoscopy, which shows severe reflux oesophagitis. He commences taking proton pump inhibitors and has good control of his symptoms.

Comment

The symptoms of cardiac ischaemia are often atypical. In the absence of recent symptoms, consideration of a cardiac cause of this patient’s presentation is essential and, in the context of this case, a single troponin test is appropriate.

Patient 5

A 58-year-old formerly well woman presents to you immediately after a 1-hour episode of burning central chest discomfort, which resolved spontaneously. She has experienced minor chest pain episodically for the past 3 days. Her physical examination and ECG are normal. It is 7 pm; you order a serum troponin test and give her a referral for an upper gastrointestinal endoscopy. As you leave the surgery, you turn off your mobile phone so that you will not be interrupted, as you are going to the cinema. When you turn your phone on later that evening, you have two messages. The first message tells you that the troponin test result showed an elevated level (hsTnI, 43 ng/L; female RI, < 16 ng/L). The second message is from your patient’s husband, who says your patient developed severe chest pain at home and they were uncertain what to do. Upon calling her husband, he tearfully says that she had a cardiac arrest at home and did not survive.

Comment

A number of concerns arise in this case. First, the troponin test should not have been ordered as there was a significant clinical suspicion of an acute coronary syndrome and, with symptoms within the past 24 hours, the patient is considered potentially at high risk and should have been urgently referred to hospital, where serial ECGs, troponin testing and risk stratification could be performed in the safety of a fully equipped emergency department. Second, whenever troponin testing is used, systems must be in place for the result to be conveyed urgently to the medical practitioner21 and appropriate action taken.

Conclusions

Acute coronary syndrome remains a major cause of death and long term morbidity. For patients presenting to a general practice with possible acute coronary syndrome within the preceding 24 hours, including symptoms consistent with either unstable angina or high risk clinical features, a serum troponin test should not be ordered. Instead, these patients should be referred to an emergency department for evaluation in a monitored environment capable of offering defibrillation, urgent fibrinolysis or revascularisation. However, patients presenting with ischaemic symptoms that occurred more than 24 hours previously, who are now symptom-free and have no high risk features, may be assessed with a single troponin assay and referred urgently to hospital if the result is elevated. If the troponin result is negative, unstable angina is not excluded and urgent or semi-urgent cardiac referral may still be appropriate, depending on the timing and severity of symptoms. When troponin assays are used, systems must be in place for the result to be conveyed urgently to a medical practitioner so that appropriate action may be taken.

Future directions

Further refinement of strategies that use high sensitivity troponin assays may improve upon the current 3-hour rule-out time for acute myocardial infarction. Other methods of early risk stratification, including imaging techniques, are currently being evaluated. In the future, troponin levels may also prove to be useful in many clinical contexts, including gauging cardiotoxicity with chemotherapeutic agents, identifying cardiac allograft rejection or monitoring patients with heart failure. In addition, there is potential for troponin testing to be included in newer models of general cardiovascular risk stratification, but until further evaluation in prospective trials demonstrates a clinical benefit, troponin should not be measured in asymptomatic individuals.

Box 1 –
Causes of serum troponin level elevation

  • Acute myocardial infarction (see )
  • Coronary artery spasm (eg, due to cocaine or methamphetamine use)
  • Takotsubo cardiomyopathy
  • Coronary vasculitis (eg, systemic lupus erythematosus, Kawasaki disease)
  • Acute or chronic heart failure
  • Tachyarrhythmia or bradyarrhythmia
  • Frequent defibrillator shocks
  • Cardiac contusion or surgery
  • Rhabdomyolysis with cardiac involvement
  • Myocarditis or infiltrative diseases (eg, amyloidosis, sarcoidosis, haemochromatosis)
  • Cardiac allograft rejection
  • Hypertrophic cardiomyopathy
  • Cardiotoxic agents (eg, anthracyclines, trastuzumab, carbon monoxide poisoning)
  • Aortic dissection or severe aortic valve disease
  • Severe hypotension or hypertension (eg, haemorrhagic shock, hypertensive emergency)
  • Severe pulmonary embolism, pulmonary hypertension or respiratory failure
  • Dialysis-dependent renal failure
  • Severe burns affecting > 30% of the body surface
  • Severe acute neurological conditions (eg, stroke, cerebral bleeding or trauma)
  • Sepsis
  • Prolonged exercise or extreme exertion (eg, marathon running)

Box 2 –
The new classification of myocardial infarction (MI)12

Type

Clinical situation

Definition


1

Spontaneous

MI related to ischaemia from primary coronary event such as plaque rupture, erosion, fissuring or dissection

2

Demand–supply imbalance

MI related to secondary ischaemia due to myocardial oxygen supply–demand imbalance such as spasm, anaemia, hypotension or arrhythmia

3

Sudden death

Unexpected cardiac death, perhaps suggestive of MI, but occurring before blood samples can be obtained

4a

PCI

MI associated with PCI procedure

4b

Stent thrombosis

MI associated with stent thrombosis, as seen on angiography or autopsy

5

CABG

MI associated with CABG


CABG = coronary artery bypass grafting. PCI = percutaneous coronary intervention.

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

Blood pressure (BP) is an important common modifiable risk factor for cardiovascular disease. In 2014–15, 6 million adult Australians were hypertensive (BP ≥ 140/90 mmHg) or were taking BP-lowering medication.1 Hypertension is more common in those with lower household incomes and in regional areas of Australia (http://heartfoundation.org.au/about-us/what-we-do/heart-disease-in-australia/high-blood-pressure-statistics). Many Australians have untreated hypertension, including a significant proportion of Aboriginal and Torres Strait Islander people.1

Cardiovascular diseases are associated with a high level of health care expenditure.2 Controlled BP is associated with lower risks of stroke, coronary heart disease, chronic kidney disease, heart failure and death. Small reductions in BP (1–2 mmHg) are known to markedly reduce population cardiovascular morbidity and mortality.3,4

Method

The National Blood Pressure and Vascular Disease Advisory Committee, an expert committee of the National Heart Foundation of Australia, has updated the Guide to management of hypertension 2008: assessing and managing raised blood pressure in adults (last updated in 2010)5 to equip health professionals across the Australian health care system, especially those within primary care and community services, with the latest evidence to prevent, detect and manage hypertension.

International hypertension guidelines68 were reviewed to identify key areas for review. Review questions were developed using the patient problem or population, intervention, comparison and outcome(s) (PICO) framework.9 Systematic literature searches (2010–2014) of MEDLINE, Embase, CINAHL and the Cochrane Library were conducted by an external organisation, and the resulting evidence summaries informed the updated clinical recommendations. The committee also reviewed additional key literature relevant to the PICO framework up to December 2015.

Recommendations were based on high quality studies, with priority given to large systematic reviews and randomised controlled trials, and consideration of other studies where appropriate. Public consultation occurred during the development of the updated guideline. The 2016 update includes the level of evidence and strength of recommendation in accordance with National Health and Medical Research Council standards10 and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology.11 No level of evidence has been included where there was no direct evidence for a recommendation that the guideline developers agreed clearly outweighed any potential for harm.

Most of the major recommendations from the guideline are outlined below, together with background information and explanation, particularly in areas of change in practice. Key changes from the previous guideline are listed in Box 1. The full Heart Foundation Guideline for the diagnosis and management of hypertension in adults – 2016 is available at http://heartfoundation.org.au/for-professionals/clinical-information/hypertension. The full guideline contains additional recommendations in the areas of antiplatelet therapy, suspected BP variability, and initiating treatment using combination therapy compared with monotherapy.

Recommendations

Definition and classification of hypertension

Elevated BP is an established risk factor for cardiovascular disease. The relationship between BP level and cardiovascular risk is continuous, therefore the distinction between normotension and hypertension is arbitrary.12,13 Cut-off values are used for diagnosis and management decisions but vary between international guidelines. Current values for categorisation of clinic BP in Australian adults are outlined in Box 2.

Management of patients with hypertension should also consider absolute cardiovascular disease risk (where eligible for assessment) and/or evidence of end-organ damage. Several tools exist to estimate absolute cardiovascular disease risk. The National Vascular Disease Prevention Alliance developed a calculator for the Australian population, which can be found at http://www.cvdcheck.org.au.

Treatment strategies for individuals at high risk of a cardiovascular event may differ from those at low absolute cardiovascular disease risk despite similar BP readings. It is important to note that the absolute risk calculator has been developed using clinic BP, rather than ambulatory, automated office or home BP measures.

Some people are not suitable for an absolute risk assessment, including younger patients with uncomplicated hypertension and those with conditions that identify them as already at high risk.14

Blood pressure measurement

A comprehensive assessment of BP should be based on multiple measurements taken on several separate occasions. A variety of methods are available, each providing different but often complementary information. Methods include clinic BP, 24-hour ambulatory and home BP monitoring (Box 3).

Most clinical studies demonstrating effectiveness and benefits of treating hypertension have used clinic BP. Clinic, home and ambulatory BP all predict the risk of a cardiovascular event; however, home and ambulatory blood pressure measures are stronger predictors of adverse cardiovascular outcomes (Box 4).15,16

Automated office BP measurement involves taking repeated blood pressure measurements using an automated device with the clinician out of the room.17,18 This technique generally yields lower readings than conventional clinic BP and has been shown to have a good correlation with out-of-clinic measures.

The British Hypertension Society provides a list of validated BP monitoring devices.19 Use of validated and regularly maintained non-mercury devices is recommended as mercury sphygmomanometers are being phased out for occupational health and safety and environmental reasons.

Treatment thresholds

Although the benefits of lowering BP in patients with significantly elevated BP have been well established, the benefit of initiating drug therapy in patients with lower BP with or without comorbidities has been less certain. A meta-analysis of patients with uncomplicated mild hypertension (systolic BP range, 140–159 mmHg) indicated beneficial cardiovascular effects with reductions in stroke, cardiovascular death and all-cause mortality, through treatment with BP-lowering therapy.20 Corresponding relative reductions in 5-year cardiovascular disease risk were similar for all levels of baseline BP.21

Decisions to initiate drug treatment at less severe levels of BP elevations should consider a patient’s absolute cardiovascular disease risk and/or evidence of end-organ damage together with accurate blood pressure readings.

Treatment targets

Optimal blood pressure treatment targets have been debated extensively. There is emerging evidence demonstrating the benefits of treating to optimal BP, particularly among patients at high cardiovascular risk.17,20

The recent Systolic Blood Pressure Intervention Trial investigated the effect of targeting a higher systolic BP level (< 140 mmHg) compared with a lower level (< 120 mmHg) in people over the age of 50 years who were identified as having a cardiovascular 10-year risk of at least 20%.17 Many had prior cardiovascular events or mild to moderate renal impairment and most were already on BP-lowering therapy at the commencement of the study. Patients with diabetes, cardiac failure, severe renal impairment or previous stroke were excluded. The method of measurement was automated office BP,18 a technique that generally yields lower readings than conventional clinic BP. Patients treated to the lower target achieved a mean systolic BP of 121.4 mmHg and had significantly fewer cardiovascular events and lower all-cause mortality compared with the other treatment group, which achieved a mean systolic level of 136.2 mmHg. Older patients (> 75 years) benefited equally from the lower target BP. However, treatment-related adverse events increased in the more intensively treated patients, with more frequent hypotension, syncopal episodes, acute kidney injury and electrolyte abnormalities.

The selection of a BP target should be based on an informed, shared decision-making process between patient and doctor (or health care provider), considering the benefits and harms and reviewed on an ongoing basis.

Recommendations for treatment strategies and treatment targets for patients with hypertension are set out in Box 5.

Box 1 –
Key changes from previous guideline

  • Use of validated non-mercury sphygmomanometers that are regularly maintained is recommended for blood pressure (BP) measurement.
  • Out-of-clinic BP using home or 24-hour ambulatory measurement is a stronger predictor of outcome than clinic BP measurement.
  • Automated office blood pressure (AOBP) provides similar measures to home and ambulatory BP, and results are generally lower than those from conventional clinic BP measurement.
  • BP-lowering therapy is beneficial (reduced stroke, cardiovascular death and all-cause mortality) for patients with uncomplicated mild hypertension (systolic BP, 140–159 mmHg).
  • For patients with at least moderate cardiovascular risk (10-year risk, 20%), lower BP targets of < 120 mmHg systolic (using AOBP) provide benefit with some increase in treatment-related adverse effects.
  • Selection of a BP target should be based on informed, shared decision making between patients and health care providers considering the benefits and harms, and reviewed on an ongoing basis.

Box 2 –
Classification of clinic blood pressure in adults

Diagnostic category*

Systolic (mmHg)

Diastolic (mmHg)


Optimal

< 120

and

< 80

Normal

120–129

and/or

80–84

High-normal

130–139

and/or

85–89

Grade 1 (mild) hypertension

140–159

and/or

90–99

Grade 2 (moderate) hypertension

160–179

and/or

100–109

Grade 3 (severe) hypertension

≥ 180

and/or

≥ 110

Isolated systolic hypertension

> 140

and

< 90


Reproduced with permission from the National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults — 2016. Melbourne: NHFA, 2016. * When a patient’s systolic and diastolic blood pressure levels fall into different categories, the higher diagnostic category and recommended actions apply.

Box 3 –
Criteria for diagnosis of hypertension using different methods of measurement

Method of measurement

Systolic (mmHg)

Diastolic (mmHg)


Clinic

≥ 140

and/or

≥ 90

ABPM daytime (awake)

≥ 135

and/or

≥ 85

ABPM night-time (asleep)

≥ 120

and/or

≥ 70

ABPM over 24 hours

≥ 130

and/or

≥ 80

HBPM

≥ 135

and/or

≥ 85


Reproduced with permission from the National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults — 2016. Melbourne: NHFA, 2016. ABPM = ambulatory blood pressure monitoring. HBPM = home blood pressure monitoring.

Box 4 –
Recommendations for monitoring blood pressure (BP) in patients with hypertension or suspected hypertension

Method of measuring BP

Grade of recommendation*

Level of evidence


If clinic BP is ≥ 140/90 mmHg or hypertension is suspected, ambulatory and/or home monitoring should be offered to confirm the BP level

Strong

I

Clinic BP measures are recommended for use in absolute cardiovascular risk calculators. If home or ambulatory BP measures are used in absolute cardiovascular disease risk calculators, risk may be inappropriately underestimated

Strong

Procedures for ambulatory BP monitoring should be adequately explained to patients. Those undertaking home measurements require appropriate training under qualified supervision

Strong

I

Finger and/or wrist BP measuring devices are not recommended

Strong


Reproduced with permission from the National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults — 2016. Melbourne: NHFA, 2016. * Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology.11 † National Health and Medical Research Council standards;10 no level of evidence included where there was no direct evidence for a recommendation that the guideline developers agreed clearly outweighed any potential for harm.

Box 5 –Recommendations for treatment strategies and treatment targets for patients with hypertension, with grade of recommendation and level of evidence*

A healthy lifestyle, including not smoking, eating a nutritious diet and regular adequate exercise is recommended for all Australians including those with and without hypertension.

  • Lifestyle advice is recommended for all patients (grade: strong; level: –).
  • For patients at low absolute cardiovascular disease risk (5-year risk, < 10%) with persistent blood pressure (BP) ≥ 160/100 mmHg, antihypertensive therapy should be started (grade: strong; level: I).
  • For patients at moderate absolute cardiovascular disease risk (5-year risk, 10–15%) with persistent systolic BP ≥ 140 mmHg and/or diastolic ≥ 90 mmHg, antihypertensive therapy should be started (grade: strong; level: I).
  • Once decided to treat, patients with uncomplicated hypertension should be treated to a target of < 140/90 mmHg or lower if tolerated (grade: strong; level: I).
  • In selected high cardiovascular risk populations where a more intense treatment can be considered, aiming for a target of < 120 mmHg systolic BP can improve cardiovascular outcomes (grade: strong; level: II).
  • In selected high cardiovascular risk populations where a treatment is being targeted to < 120 mmHg systolic BP, close follow-up of patients is recommended to identify treatment-related adverse effects including hypotension, syncope, electrolyte abnormalities and acute kidney injury (grade: strong; level: II).
  • In patients with uncomplicated hypertension, angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs), calcium channel blockers and thiazide diuretics are all suitable first-line antihypertensive drugs, either as monotherapy or in some combinations unless contraindicated (grade: strong; level: I).
  • The balance between efficacy and safety is less favourable for β-blockers than other first-line antihypertensive drugs. Thus β-blockers should not be offered as a first-line drug therapy for patients with hypertension that is not complicated by other conditions (grade: strong; level: I).
  • ACE inhibitors and ARBs are not recommended in combination due to an increased risk of adverse effects (grade: strong; level: I).

Treatment-resistant hypertension

Treatment-resistant hypertension is defined as a systolic BP ≥ 140 mmHg in a patient who is taking three or more antihypertensive medications, including a diuretic at optimal tolerated doses. Contributing factors may include variable compliance, white coat hypertension or secondary causes for hypertension.Few drug therapies specifically target resistant hypertension. Renal denervation is currently being investigated as a treatment option in this condition; however, to date, it has not been found to be effective in the most rigorous study conducted.22

  • Optimal medical management (with a focus on treatment adherence and excluding secondary causes) is recommended (grade: strong; level: II).
  • Percutaneous transluminal radiofrequency sympathetic denervation of the renal artery is currently not recommended for the clinical management of resistant hypertension or lower grades of hypertension (grade: weak; level: II).

Patients with hypertension and selected comorbidities

Stroke and transient ischaemic attack:

  • For patients with a history of transient ischaemic attacks or stroke, antihypertensive therapy is recommended to reduce overall cardiovascular risk (grade: strong; level: I).
  • For patients with a history of transient ischaemic attacks or stroke, any of the first-line antihypertensive drugs that effectively reduce BP are recommended (grade: strong; level: I).
  • For patients with hypertension and a history of transient ischaemic attacks or stroke, a BP target of < 140/90 mmHg is recommended (grade: strong; level: I).

Chronic kidney disease:

Most classes of BP-lowering drugs have a similar effect in reducing cardiovascular events and all-cause mortality in patients with chronic kidney disease (CKD). When treating with diuretics, the choice should be dependent on both the stage of CKD and the extracellular fluid volume overload in the patient. Detailed recommendations on how to manage patients with CKD are available.23

  • In patients with hypertension and CKD, any of the first-line antihypertensive drugs that effectively reduce BP are recommended (grade: strong; level: I).
  • When treating hypertension in patients with CKD in the presence of microalbuminuria or macroalbuminuria, an ARB or ACE inhibitor should be considered as first-line therapy (grade: strong; level: I).
  • In patients with CKD, antihypertensive therapy should be started in those with BP consistently > 140/90 mmHg and treated to a target of < 140/90 mmHg (grade: strong; level: I).
  • Dual renin-angiotensin system blockade is not recommended in patients with CKD (grade: strong; level: I).
  • For patients with CKD, aiming towards a systolic BP < 120 mmHg has shown benefit, where well tolerated (grade: strong; level: II).
  • In people with CKD, where treatment is being targeted to less than 120 mmHg systolic BP, close follow-up of patients is recommended to identify treatment-related adverse effects, including hypotension, syncope, electrolyte abnormalities and acute kidney injury (grade: strong; level: I).
  • In patients with CKD, aldosterone antagonists should be used with caution in view of the uncertain balance of risks versus benefits (grade: weak; level: –).

Diabetes:

  • Antihypertensive therapy is strongly recommended in patients with diabetes and systolic BP ≥ 140 mmHg (grade: strong; level: I).
  • In patients with diabetes and hypertension, any of the first-line antihypertensive drugs that effectively lower BP are recommended (grade: strong; level: I).
  • In patients with diabetes and hypertension, a BP target of < 140/90 mmHg is recommended (grade: strong; level: I).
  • A systolic BP target of < 120 mmHg may be considered for patients with diabetes in whom prevention of stroke is prioritised (grade: weak; level: –).
  • In patients with diabetes, where treatment is being targeted to < 120 mmHg systolic BP, close follow-up of patients is recommended to identify treatment-related adverse effects including hypotension, syncope, electrolyte abnormalities and acute kidney injury (grade: strong; level: –).

Myocardial infarction:

  • For patients with a history of myocardial infarction, ACE inhibitors and β-blockers are recommended for the treatment of hypertension and secondary prevention (grade: strong; level: II).
  • β-Blockers or calcium channel blockers are recommended for symptomatic patients with angina (grade: strong; level: II).

Chronic heart failure:

  • In patients with chronic heart failure, ACE inhibitors and selected β-blockers are recommended (grade: strong; level: II).
  • ARBs are recommended in patients who do not tolerate ACE inhibitors (grade: strong; level: I).

Peripheral arterial disease:

  • In patients with peripheral arterial disease, treating hypertension is recommended to reduce cardiovascular disease risk (grade: strong; level: –).
  • In patients with hypertension and peripheral arterial disease, any of the first-line antihypertensive drugs that effectively reduce BP are recommended (grade: weak; level: –).
  • In patients with hypertension and peripheral arterial disease, reducing BP to a target of < 140/90 mmHg should be considered and treatment guided by effective management of other symptoms and contraindications (grade: strong; level: –).

Older people:

  • Any of the first-line antihypertensive drugs that effectively reduce BP can be used in older patients with hypertension (grade: strong; level: I).
  • When starting treatment in older patients, drugs should be commenced at the lowest dose and titrated slowly as adverse effects increase with age (grade: strong; level: –).
  • For patients > 75 years of age, aiming towards a systolic BP of < 120 mmHg has shown benefit, where well tolerated, unless there is concomitant diabetes (grade: strong; level: II).
  • In older people whose treatment is being targeted to < 120 mmHg systolic BP, close follow-up is recommended to identify treatment-related adverse effects including hypotension, syncope, electrolyte abnormalities and acute kidney injury (grade: strong; level: II).
  • Clinical judgement should be used to assess benefit of treatment against risk of adverse effects in all older patients with lower grades of hypertension (grade: strong; level: –).

Adapted with permission from the National Heart Foundation of Australia. Guideline for the diagnosis and management of hypertension in adults – 2016. Melbourne: NHFA, 2016. * Grade of recommendation based on the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology;11 level of evidence according to the National Health and Medical Research Council standards10 — no level of evidence included where there was no direct evidence for a recommendation that the guideline developers agreed clearly outweighed any potential for harm.

Commonly used drugs that can exacerbate heart failure

The American Heart Association have released their first scientific statement which outlines which commonly used medications and nutritional supplements could worsen or cause heart failure.

It helps medical professionals and patients avoid drug-drug or drug-condition interactions and provides information about natural supplements and remedies that could injure the heart.

Heart failure patients have an average of five or more medical conditions and could be on seven or more medications, all prescribed by different doctors.

“Since many of the drugs heart failure patients are taking are prescribed for conditions such as cancer, neurological conditions or infections, it is crucial but difficult for healthcare providers to reconcile whether a medication is interacting with heart failure drugs or making heart failure worse,” said Robert L. Page II, Chair of the writing committee for the new statement published in the AHA journal Circulation.

Related: MJA – Primary prevention of cardiovascular disease: new guidelines, technologies and therapies

Common over-the-counter NSAIDs and cold and flu preparations are included in the list of drugs that can damage the heart.

As many of these medications have high sodium content, they could exacerbate heart failure.

“For example, many cough, cold, and allergy and sinus preparations may have NSAIDs such as ibuprofen or vasoconstrictors such as phenylephrine or pseudoephedrine. Because both phenylephrine and pseudoephedrine exert their effects on adrenergic receptors, cardiotoxicity such as myocardial ischemia, MI, stroke, and arrhythmias can be seen with high dose and prolonged, excessive use,” the authors wrote.

When it comes to complementary and alternative medicine (CAMs), there is little quality efficacy or safety data to back up their use, Despite this, 38% of American adults use alternative medicines.

Related: Some things you should know about statins and heart disease

The authors say ‘natural’ products such as aconite, ginseng, gossypol, St John’s wort, green tea and licorice could be harmful in patients with heart failure or could interfere with heart failure medications.

Dr Page said patients need to be more vigilant about reading labels.

“Patients have been taught to read food labels for sodium content, but they also need to read labels on over-the-counter medications and natural supplements,” he said.

Healthcare providers should also conduct a comprehensive medication reconciliation at each clinical visit.

“Patients should be specifically asked about drug, dose, and frequency of all their medications, including OTC medications and CAMs,” the authors advised.

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Diabetes drug lowers risk of heart attack, stroke

A glucose-lowering drug has been shown to safely lower the overall risk of heart attack, stroke or cardiovascular death among type 2 diabetes patients.

Patients who were at risk for cardiovascular disease were found to have a 13% lower risk of cardiovascular death, non-fatal heart attack or non-fatal stroke when they took the drug Liraglutide compared to those who took placebo.

The randomised, double-blind study assigned patients either liraglutide or placebo and followed them for an average of 3.8 years.

Study results found a 22% lower risk of cardiovascular mortality, 15% risk of all-cause mortality and 22% lower risk of new evidence of advanced diabetic kidney disease.

Related: Call for gastric surgery to treat diabetes

“It is exciting to see such a broad-based benefit for patients who took liraglutide because most prior trials of diabetes medications have not shown such benefits,” lead investigator John B. Buse from the University of North Carolina School of Medicine said.

“Our results should give patients and providers comfort that liraglutide can safely improve outcomes beyond the core treatment of type 2 diabetes.”

The results were presented at the American Diabetes Association’s 76th Scientific Sessions in New Orleans over the weekend and were published in the New England Journal of Medicine.

In another study presented published in NEJM, it was found that empagliflozin was associated with slower progression of kidney disease and lower rates of clinically relevant renal events in patients with type 2 diabetes at high risk for cardiovascular event.

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