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Cardiology

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Dr Linda Calabresi
Clinical Articles iconClinical Articles

Pass the salt

Salt may have been unfairly targeted as a killer in the healthy heart stakes, according to newly published research. The observational study of over 90000 people in 300 communities across 18 countries, found that sodium consumption was not associated with an increase in health risks unless the average daily consumption was excessive – more than 5g/day or 2.5 teaspoons of salt. And, this average high daily sodium intake was mostly seen in China, with only about 15% of communities outside of China exceeding this 5g a day limit. As part of this ongoing Prospective Urban Rural Epidemiology (PURE) study, participants aged 35-70 were assessed initially at baseline and then followed for an average of 8.1 years, over which time the occurrence of any major cardiovascular events or death was recorded. What the researchers found was that the risk of hypertension and strokes was only increased in communities where the average daily sodium intake was greater than 5g. Perhaps unexpectedly, this higher sodium intake was actually found to be also associated with lower rates of myocardial infarction and total mortality. Furthermore, the research found that very low levels of sodium intake were harmful, being associated with an increased risk of cardiovascular disease and mortality. The findings fly in the face of the current WHO guidelines that recommend, as a global approach we should be aiming for populations to reduce their sodium intake to below 2g/day. However, no communities in the study came close to achieving this target. In fact, no communities in the study had an average sodium intake of less than 3g/day, based on morning fasting urine samples from the participants. “Sodium intake was associated with cardiovascular disease and strokes only in communities where mean intake was greater than 5g/day. A strategy of sodium reduction in these communities and countries but not in others might be appropriate,” the Canadian study authors said. But before we all go and stock up on our Saxa, an accompanying editorial sounds a word of caution. While acknowledging the findings that ‘normal’ salt intake appeared to be at least health-neutral if not beneficial, the editorial authors remind us that the study is observational and has not taken into consideration a number of potential confounders such as diet. Without taking these confounders into account, one can’t assume that just decreasing salt intake in people at high risk of stroke or increasing it in people at risk of a heart attack will work, they said. “Nevertheless the findings are exceedingly interesting and should be tested in a randomised controlled trial,” they concluded, adding that such a trial, to be conducted in a US federal prison population had been proposed.   Ref: Lancet Vol 392 No 10146 pp:496-506 Vol 392 No 10146 pp: 456-458

Expert/s: Dr Linda Calabresi
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Dr Linda Calabresi
Clinical Articles iconClinical Articles

LDL – The Lower the Better

Low density lipoprotein cholesterol is the well-known culprit in terms of cardiovascular risk. Courtesy of a large meta-analysis of statin trials done in 2010 (the Cholesterol Treatment Trialists Collaboration), we know that for people starting with higher LDL-C levels (approximately 3.4 mmol/L), they can lower their risk of having a major adverse vascular event by 22%, every time they lower their LDL-C level by 1mmol/L. But what happens once your LDL level is lower? Can you continue to increase your protection by lowering your LDL levels further? Or does the beneficial effect plateau at a certain level? Or, worse still can very low LDL levels actually cause harm? A new meta-analysis just published in JAMA Cardiology has gone some way in answering these questions. The researchers analysed data from the 26 statin studies in the CTTC as well as three large trials of non-statin, cholesterol-lowering therapy looking at those patients who had an LDL-C level of 1.8 mmol/L or less at baseline. They found the cardioprotective benefits continued as LDL-C levels declined to even lower levels. “We found consistent clinical benefit from further LDL-C lowering in patient populations starting as low as a median of 1.6 mmol/L and achieving levels as low as a median of 0.5 mmol/L”. What’s more, the incremental benefit was of an almost identical magnitude to that seen when the LDL-C levels were higher - 21% relative risk reduction per 1-mmol/L reduction in LDL-C through this range. “This relative risk reduction is virtually the same as the 22% reduction seen in the overall CTTC analysis in which the starting LDL-C was nearly twice as high,” they said. And even though very low cholesterol levels have been rumoured to be associated with everything from cancer to dementia, across all these studies there were no offsetting safety concerns with LDL-C lowering, even when extremely low levels were recorded, levels that were lower than those seen in newborns. Given the weight of benefit over risk, the study authors suggest the current targets for LDL-C could be lowered further, to even as low as 0.5 mmol/L to reduce cardiovascular risk. This suggestion is supported by an accompanying editorial, in which the author, Dr Antonio Gotto, a New York cardiologist, predicts the findings will be included as part of the revision of the American Heart Association National Cholesterol guidelines which is currently underway. He said the study findings would provide much needed evidence to help clinicians manage patients with these extremely low achieved cholesterol levels, that until recently have been very rare. “Whether one calls it a target or a threshold, practicing physicians need some guidance as they venture into achieved levels of LDL-C levels that are as foreign as travel to outer space. I have confidence that the new guidelines will be closer to a global positioning system map rather than just a compass and the stars”, he concluded. Ref: JAMA Cardiol. Published online August 1, 2018. doi:10.1001/jamacardio.2018.2258

Expert/s: Dr Linda Calabresi
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Dr Linda Calabresi
Clinical Articles iconClinical Articles

Treating depression in MI patients saves lives

Effectively treating depression in patients who have just experienced a heart attack will not only improve their quality of life, it could well improve their mortality, new research from Korea suggests. Among 300 patients who had recently experienced acute coronary syndrome and had depression as a comorbidity, those randomised to a 24-week course of escitalopram were 30% less likely to have a major adverse cardiac event over a median of eight years compared with those given placebo. In actual numbers, 40.9% (61)of the 149 patients given escitalopram had a major adverse event (including cardiac death, MI or PCI) over the period of follow-up compared with 53.6% (81) of the placebo group (151 patients), according to the study findings published in JAMA. It has long been known that depression is a common morbidity associated with acute coronary syndrome. It is also known that patients who have this comorbidity tend to have worse long-term cardiac outcomes than those who are depression-free. But what has yet to be proven is the benefit of treating this depression, at least in terms of mitigating this increased risk of a poor cardiac outcome. To date studies on the topic have yet to prove a significant benefit, with research providing conflicting results. According to the study authors, in this trial there was a significant correlation between improvement in the depression and better protection against major cardiac events. Even when they excluded those people who were still taking the antidepressant one year after the acute coronary syndrome, the protective effect was still present. Consequently, they hypothesised that the protection was more a reflection of the successfully treatment of the depression rather than the particular medication. This was consistent with a trend seen in previous research using different medications and treatments. However, the better result could be because escitalopram is more effective in treating acute coronary syndrome depression than other agents that were studied previously, the authors suggested. “Escitalopram may have modifying effects on disease prognosis in ACS-associated depressive disorder through reduction of depressive symptoms,” the study authors suggested. There were a number of caveats with regard this study that the authors said needed to be considered. These included the fact the cohort was entirely Korean which may have caused an ethnic bias, the depressive symptoms were less severe than in previous studies (though this was more likely to lead to the effect being an under-estimate) and also the severity of the underlying heart disease (namely heart failure) was relatively low. Nonetheless the researchers were able to conclude that among patients with depression who had had a recent acute coronary event, 24 weeks of treatment of escitalopram significantly reduced the risk of dying or having a further adverse cardiac event after a median of 8.1 years. How generalisable these findings are, will need to be the subject of further research. Ref: JAMA 2018;320 (4): 350-357. Doi: 10.1001/jama.2018.9422

Expert/s: Dr Linda Calabresi
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Dr Linda Calabresi
Clinical Articles iconClinical Articles

Diagnosed with hypertension? Think aldosteronism

All newly-diagnosed hypertensive patients should be screened for primary aldosteronism before they are started on treatment, Australian experts suggest in the latest issue of the MJA. “Primary aldosteronism is common, specifically treatable, and associated with significant cardiovascular morbidity and mortality,” say researchers Dr Jun Yang, Professor Peter Fuller and Professor Michael Stowasser. They refer to a recent systematic review of over 30 studies, that found among a cohort of people with severe or resistant hypertension (systolic BP >180mmHg and diastolic BP >110), 16.4% were found to have primary aldosteronism. Admittedly these studies were carried out in tertiary centres. There been far fewer studies on the issue conducted in primary care with somewhat mixed results, with one small Australian study suggesting 11.5% of people with significant hypertension in the general practice setting had primary aldosteronism. But its not only the patients with severe hypertension that need to be considered for primary aldosteronism screening, the authors suggest. They point to an Italian study including over 1600 GP patients selected randomly who were screened for primary aldosteronism and found a prevalence of 5.9%.  Importantly 45% of these had mild hypertension (BP 140-159/90-99mmHg). According to the article authors, these patients, because would have most likely remained undiagnosed if not for the study. And the effect of the untreated aldosterone excess would have most likely led to poor blood pressure control and increased cardiovascular, renal and metabolic morbidity long-term. In other words, identifying these patients early in the course of the disease could allow more appropriate treatment and ultimately avoid the end-organ damage that is more likely to occur if diagnosis is delayed until after the development of severe hypertension. “Targeted treatment of [primary aldosteronism] using surgery or mineralocorticoid receptor antagonists, such as spironolactone and eplerenone, rather than non-specific antihypertensive medications, can reverse the underlying cardiovascular pathology,” they said. The recommended biochemical screening tool for primary aldosteronism is the aldosterone to renin ratio which is elevated in this condition because plasma aldosterone is normal or elevated while renin is suppressed. The experts suggest screening prior to commencing antihypertensive therapy as many of these drugs, including beta blockers, calcium channel blockers, ACE inhibitors, ARBs and diuretics usually interfere with this aldosterone to renin ratio. The test isn’t perfect, they admit, as it can be influenced by a number of confounders including salt intake and age, but as a screening tool it has been proven, in trials both in Australia and internationally to be very useful, resulting in significantly increased numbers of patients diagnosed. Current Australian hypertension guidelines recommend clinicians consider primary aldosteronism in patients with hypertension particularly those with moderate to severe or treatment-resistant hypertension. But, as the article authors point out, given the prevalence of primary aldosteronism and the health burden associated with this cardiovascular risk factor both to the Australian population and the economy, maybe it is time to consider screening all newly-diagnosed hypertensive patients for this condition, before the commencement of non-specific antihypertensive therapy. “This diagnostic strategy should lead to significant individual and population health and economic impacts as a result of many patients with hypertension being offered the chance of curative or simpler treatment at an early stage of their disease.” Ref: MJA doi:10.5694/mja17.00783

Expert/s: Dr Linda Calabresi
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Dr Vivienne Miller
Clinical Articles iconClinical Articles

An Update in Heart Failure

How easy is it to say HFpEF and HFrEF?   The answer is… not very easy! However, heart failure has a new classification based on ejection fraction that doctors will need to know about. HFpEF stands for “heart failure with preserved ejection fraction.” This preserved ejection fraction is defined as greater than or equal to 50%. HFrEF stands for “heart failure with reduced ejection fraction.” This is the “classic” form of heart failure that doctors are familiar with. The ejection fraction in HRrEF is defined as less than or equal to 50%. Patients who have clinical signs of heart failure and a normal ejection fraction used to be diagnosed with diastolic heart failure.  They are now said, under the new classification, to have HFpEF. It should be noted that a patient may have diastolic dysfunction typically reported on echo, however if they do not have any clinical signs of heart failure they do NOT have HFpEF. In this situation, the diastolic dysfunction refers to the cardiac echo finding of impaired diastolic relaxation. This may be an age-related change or due to left ventricular hypertrophy, both of which may occur without necessarily causing symptoms and signs of heart failure. There is an additional group that some researchers refer to, and that is HFmEF, which stands for “heart failure with mid-range ejection fraction”. HFmEF is defined as an ejection fraction of between 40% and 50%. There is debate about the utility of the additional sub-classification of HFmEF. Most clinicians would consider HFmEF as simply mild HFrEF. Most agree that HFmEF simply identifies as subgroup of HFrEF for which there are fewer clinical trials or evidence for effective therapy, and so this highlights areas for future investigation and research. The utility of this new classification, particularly HFrEF versus HFpEF, is mainly to distinguish different pathophysiological processes, cardiac mechanics and treatment options. Presently, it is only HFrEF for which there exists medications that reduce mortality and improve survival. Additionally, device therapies such as implantable cardioverter defibrillators and biventricular pacemakers (now more commonly referred to as “cardiac resynchronisation therapies”) have only demonstrated benefit in HFrEF. For HFpEF, there are no medications or devices that have been shown to reduce mortality and improve survival. Typically, symptoms are managed with diuretic therapy. There is evidence to support a benefit from spironolactone, however the most recent trial (TOPCAT)1 failed to demonstrate a mortality benefit and it was plagued with disparities regarding the nature of recruitment in one of the large regions participating. Certainly, from a treatment viewpoint, the underlying causes contributing to HFpEF can often be managed. These typically include hypertension, diabetes, obesity and coronary artery disease. Not surprisingly, there are studies to show that patients with HFpEF do benefit from exercise, and from maintaining a healthy weight. But how best do we explain these definitions to the patient sitting in front of us? 'It can be very helpful to clarify the term [heart failure] and to explain that their heart has neither “failed”, nor has it “stopped working”, but that “it is just not working as well as normal”, said cardiologist, Dr Hendrik Zimmet. HFrEF can be explained as “the heart muscle not pumping as well as usual”. HFpEF can be explained as “the heart muscle being stiffer than usual, and not relaxing as well”. But no matter how the problem is explained to the patient, it is important to stress, as positively as possible, what can be done to help.
  1. Pfeffer, Marc et al. Regional Variation in Patients and Outcomes in the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) Trial
Circulation. 2014; CIRCULATIONAHA.114.013255 Originally published November 18, 2014 https://doi.org/10.1161/CIRCULATIONAHA.114.013255 Based on an interview with cardiologist, Dr Hendrik Zimmet at the Annual Women and Children’s Health Update, Melbourne, March 2018

Expert/s: Dr Vivienne Miller
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Dr Christopher Reid
Monographs iconMonographs

The Role of Low Dose Aspirin in the Secondary Prevention of Cardiovascular Disease

This article discusses the evidence for and role of aspirin in the secondary prevention of cardiovascular events following the clinical manifestation of atherosclerotic disease.

Expert/s: Dr Christopher Reid, Dr Adeleh Shirangi
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Dr Linda Calabresi
Clinical Articles iconClinical Articles

Omega-3 fatty acids do not prevent heart attacks

Taking fish oil supplements to prevent a heart attack has always been somewhat controversial. However, a new meta-analysis, involving almost 78,000 high risk individuals has provided the best evidence to date that the practice is not worthwhile. (1) The UK researchers analysed the data from 10 trials which had investigated whether taking omega-3 fatty acid supplementation reduced the risk of fatal and non-fatal coronary heart disease as well as other vascular events including stroke. According to the study findings, published in JAMA Cardiology, those individuals randomised to omega-3 fatty acid supplementation for a mean of 4.4 years experienced no significant benefit in terms of preventing adverse vascular outcomes compared with those who did not receive supplementation. “Importantly, this meta-analysis also demonstrated no significant effect on major vascular events in any particular sub-groups, including prior vascular disease, diabetes, lipid levels, or statin use,” the study authors wrote. They suggest that the results of this study provide no support for the recommendations to use approximately 1g/d of omega-3 fatty acids in patients with a history of coronary heart disease to prevent heart attacks or any other vascular disease, which is the current advice from American Heart Association. Our own Australian Heart Foundation guidelines have been a little more circumspect with regard omega-3 fatty acids. While they do suggest supplementation for people whose diet is lacking in fish sources of EPA and DHA, they do say the cardioprotective benefit may be only for some high-risk groups. “There is evidence omega-3 supplements can play a beneficial role in the treatment of patients with high triglyceride levels and patients with existing heart disease, specifically heart failure,” according to their website. (2) Whether this advice is set to change remains to be seen. However, while this latest study might seem like the nail in the coffin for the fish oil business there is an important caveat to consider. The trials included in the meta-analysis involved various doses of omega-3 fatty acid supplementation. All but one trial included combinations of EPA and DHA, with the one exception being a trial of EPA supplementation alone. Daily doses of EPA ranged from 226 to 1800 mg/day and DHA doses varied from 0 to 1700mg/day. Several large randomised controlled trials, involving over 50,000 participants are currently underway investigating whether much higher doses of omega-3 fatty acids will reduce the risk of major cardiovascular events. Even the authors of this latest meta-analysis concede “The results of the ongoing trials are needed to assess if higher doses of omega-3 fatty acids (3-4g/d) may have significant effects on risk of major vascular events.” Ref: 1. JAMA Cardiol. doi: 10.1001/jamacardio.2017.5205 2. https://www.heartfoundation.org.au/images/uploads/main/Programs/Health_Professional_QA_Fish_Omega3_Cardiovascular_Health.pdf

Expert/s: Dr Linda Calabresi
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Dr Linda Calabresi
Clinical Articles iconClinical Articles

Pressure increased on hypertension treatment

New US guidelines are the most aggressive yet in terms of targets for blood pressure control. Put out by the American College of Cardiology and the American Heart Association, and published in JAMA, the guidelines recommend we now consider anyone with a BP of 120/80 mmHg or above as having abnormal blood pressure. People who have a systolic between 120 and 130 mmHg but whose diastolic is still below 80 mmHg are to be considered to have elevated BP. But those who have both a systolic up to 10mmHg above target (120-130mmHg) and a diastolic between 80 and 90 mmHg should now be classified as having stage 1 hypertension. An accompanying editorial estimates that this reclassification will result in a 14% increase in the US population who should be recognised as having hypertension. But before clinicians start reaching for the script pad, the guidelines recommend this stage 1 hypertension be initially treated with non-pharmacological therapies – basically addressing the factors that most likely pushed their blood pressure up to start with – lose weight, exercise more, reduce salt intake, cut down on alcohol. The exception to this, is that group of patients whose absolute 10 year CVD risk predictor has them with a 10% or more chance of having a major CV event. In these cases, it’s gloves off. The less than 130/80 target for high risk patients is very similar to Australian guidelines. What’s different is that this is now a recommended target for everyone. The new US guidelines recommend everyone with a BP over 140/90 mmHg be treated with medication (preferably two agents) regardless of their absolute CV risk. Our Heart Foundation says try other lifestyle changes in people with a very low CV risk and no other comorbidities until we reach the 160/100 mmHg mark. The other new development in the US guidelines is the recommendation to use BP measurements from ambulatory or home BP monitoring to both confirm a diagnosis of hypertension and titrate therapy. This is in keeping with Australian recommended practice. The US guidelines were developed by an expert committee after examining all the current evidence and conducting a series of systematic reviews looking at some key clinical questions. “From a public health perspective, considering the high population-attributable risk of CVD associated with hypertension, the potential benefits of tighter control of hypertension are substantial,” the guideline authors wrote. However, they do acknowledge that such an aggressive approach does carry risks, especially in the elderly. “Although studies do suggest that lower BP is better for most patients, including those older than 75 years, the balance of the potential benefits of hypertension management and medication costs, adverse effects, and polypharmacy must be considered for each individual patient,” they said. Ref: JAMA. Published online November 20, 2017. doi:10.1001/jama.2017.18706

Expert/s: Dr Linda Calabresi
Just Checking people with an intellectual disability
Dr Lee Price
Clinical Articles iconClinical Articles

Measuring Troponin In General Practice

High sensitivity(HS) troponin measurement in the emergency room/hospital setting is now widely established in Australia and is now being recommended for widespread implementation in the USA. Lower cut-offs into the normal range may find value as a single determinant for exclusion purposes in the acute emergency ward setting, however, because HS troponin may be elevated in a number of noncoronary cardiac conditions, a rise and/or fall in the level is usually required for diagnosis of a coronary infarct1. In unstable angina pectoris, a troponin level may be normal, as may an ECG recording if the patient is pain free at the time. Two articles in the Medical Journal of Australia published in the past three years have addressed the issues/problems surrounding ordering of the test in general practice 1,2. In both articles the authors agree that there are times when a single measurement of HS troponin can be useful clinically; however, there are times when it can be counterproductive. Firstly, it is agreed that a patient with classical features of the acute coronary syndrome (ACS) plus or minus ECG findings who has had pain in the 24 hours prior to assessment should be referred urgently to an emergency centre without troponin measurement. The turnaround time for an urgent troponin in most acute hospitals is of the order of 60 minutes or less. In the community private pathology scenario, turnaround time for a troponin result, even when treated as urgent, could take anywhere from four to 12 hours. That usually means that the result is only available after hours. Frequently, the ordering clinician is unavailable to receive or act on the result. A troponin can be useful in the general practice setting if the patient has had atypical chest pain with a low but not negligible likelihood of ACS; or if the patient has been pain and symptom free for 24 hours with a normal ECG. After an infarct, troponin can remain elevated for over a week. For the laboratory, an abnormal troponin requires phoning the result if it is an urgent request from the clinician. This may be after hours – even after midnight. Usually the context of the result is only known by the requesting clinician. If a requesting clinician is unavailable to receive the result after hours, the patient will usually be contacted by a pathologist or emergency services. After-hours doctor services often are uninterested in receiving or acting on critical results such as troponin. In summary, there is a place for troponin measurement in general practice. Elevated levels are not uncommon due to causes other than the ACS. Turnaround time for a result may take much longer when collected in a collection centre than in the hospital setting. When ordering an urgent troponin please ensure that the laboratory has a valid contact number for after hours. References 1. Aroney CA, Cullen L. Appropriate use of serum troponin testing in general practice: a narrative review. MJA 2016; 205:(2) 91-94. 2. Marshall GA, Wijeratne NG, Thomas D. Should general practitioners order troponin tests? MJA 2014; 201: 155-157.
General Practice Pathology is a new regular column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.

Expert/s: Dr Lee Price
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Dr Joyce Wu
Clinical Articles iconClinical Articles

New Guidance For Assessment Of Lipids

Non-fasting specimens are now acceptable Fasting specimens have traditionally been used for the formal assessment of lipid status (total, LDL and HDL cholesterol and triglycerides). In 2016, the European Atherosclerosis Society and the European Federation of Clinical Chemistry and Laboratory Medicine released a joint consensus statement that recommends the routine use of non-fasting specimens for the assessment of lipid status.2 Large population-based studies were reviewed which showed that for most subjects the changes in plasma lipids and lipoproteins values following food intake were not clinically significant. Maximal mean changes at 1–6 hours after habitual meals were found to be: +0.3 mmol/L for triglycerides; -0.2 mmol/L for total cholesterol; -0.2 mmol/L for LDL cholesterol; -0.2 mmol/L for calculated non-HDL cholesterol and no change for HDL cholesterol. Additionally, studies have found similar or sometimes superior cardiovascular disease risk associations for non-fasting compared with fasting lipid test results. There have also been large clinical trials of statin therapy, monitoring the efficacy of treatment using non-fasting lipid measurements. Overall, the evidence suggests that non-fasting specimens are highly effective in assessing cardiovascular disease risk and treatment responses.

Non-HDL cholesterol as a risk predictor

In the 2016 European joint consensus statement2 and in previously published guidelines and recommendations, the clinical utility of non-HDL cholesterol (calculated from total cholesterol minus HDL cholesterol) has been noted as a predictor of cardiovascular disease risk. Moreover, this marker has been found to be more predictive of cardiovascular risk when determined in a non-fasting specimen.

What this means for your patients

The assessment of lipid status with a non-fasting specimen has the following benefits:
  • No patient preparation is required, thereby reducing non-compliance
  • Greater convenience with attendance for specimen collection at any time
  • Reports are available for earlier review instead of potential delays associated with obtaining fasting results

Indications for repeat testing or a fasting specimen collection

For some patients, lipid testing on more than one occasion may be necessary in order to establish their baseline lipid status. It is also important to note that an assessment of lipid status carried out in the presence of any intercurrent illness may not be valid. Conditions for which a fasting specimen collection is recommended2 include:
  • Non-fasting triglyceride >5.0 mmol/L
  • Known hypertriglyceridaemia followed in a lipid clinic
  • Recovering from hypertriglyceridaemic pancreatitis
  • Starting medications that may cause severe hypertriglyceridaemia (e.g., steroid, oestrogen, retinoid acid therapy)
  • Additional laboratory tests are requested that require fasting or morning specimens (e.g., fasting glucose, therapeutic drug monitoring)

Lipid reference limits and target levels for treatment are under review

The chemical pathology community in Australia is currently reviewing all relevant publications in order to implement a consensus approach to reporting and interpreting lipid results. This includes the guidelines for management of absolute cardiovascular disease risk developed by the National Vascular Disease Prevention Alliance (NVDPA).3

Further information

  • Absolute cardiovascular disease risk calculator is available atwww.cvdcheck.org.au
  • If familial hypercholesterolaemia is suspected, e.g. LDL cholesterol persistently above 5.0 mmol/L in adults, then advice about diagnosis and management is available at www.athero.org.au/fh
References
  1. Rifai N, et al. Non-fasting Sample for the Determination of Routine Lipid Profile: Is It an Idea Whose Time Has Come? ClinChem 2016;62: 428-35.
  2. Nordestgaard BG, et al. Fasting Is Not Routinely Required for Determination of a Lipid Profile: Clinical and Laboratory Implications Including Flagging at Desirable Concentration Cutpoints -A Joint Consensus Statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. Clin Chem 2016;62: 930-46.
  3. National Vascular Disease Prevention Alliance, Absolute cardiovascular disease management, Quick reference guide for health professionals
General Practice Pathology is a new fortnightly column each authored by an Australian expert pathologist on a topic of particular relevance and interest to practising GPs. The authors provide this editorial, free of charge as part of an educational initiative developed and coordinated by Sonic Pathology.
Expert/s: Dr Joyce Wu, Dr Nick Taylor

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