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Cardiology

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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
Feature image #20
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
heart attack stroke
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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