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Press Releases

Take a look at a selection of our recent media coverage:

Ultrahigh resolution CT enables coronary artery disease diagnosis in high-risk patients

29th June 2023

A study by German researchers has shown that an ultrahigh resolution coronary CT angiography can enable clinicians to diagnose coronary artery disease in high-risk patients prior to transcatheter aortic value replacement.

Patients with severe aortic stenosis and who are suitable for transcatheter aortic valve replacement (TAVR), often have co-existing coronary artery disease (CAD). Moreover, guidelines recommend that patients suitable for TAVR undergo an assessment for CAD. Although coronary CT angiography can be used to assess the whether a patient has CAD, it often overestimates the extent of disease in high-risk patients. With the introduction of ultrahigh resolution coronary CT angiography, it may be possible to identify CAD in these high-risk patients.

Writing in the journal Radiology, the German team set out to determine the diagnostic accuracy of the new ultrahigh resolution coronary CT angiography for the detection of CAD compared with the reference standard of invasive coronary angiography (ICA).

The team examined participants with severe aortic valve stenosis and who were clinically indicated for transcatheter aortic valve replacement. All participants underwent ultrahigh-resolution photon-counting CT angiography and invasive coronary angiography, with the latter being part of their clinical care. The image quality was assessed on a 5-point Likert scale, where one was excellent and five non-diagnostic.

In addition, clinicians, who were blind to the ICA findings, assessed for the presence of CAD, defined by a 50% or greater stenosis. The ultrahigh resolution CT and ICA findings were compared using area under the receiver operating characteristic curve (AUC).

Diagnostic accuracy of the ultrahigh resolution CT

A total of 68 patients (mean age 81 years, 52.9% female) with severe aortic valve stenosis and an indication for TAVR were included in the comparative analysis. The median image quality score was 1.5 with most segments rated as either good or excellent quality.

The ultrahigh resolution CT AUC for the detection of CAD was 0.93 (95% CI 0.86 – 0.99) at the participant level, 0.94 (95% CI 0.91 – 0.98) at the vessel level and 0.92 (95% CI 0.87 – 0.97) at the segment level. This gave rise to a 96% sensitivity, an 84% specificity and 88% accuracy for the detection of coronary artery disease.

Although seemingly impressive results, the researchers called for confirmatory research with more subjects to improve the generalisability of their findings, as well as larger trials with patient-related end points to determine the potential clinical benefits of photon-counting CT.

Wine drinking associated with reduced risk of adverse cardiovascular outcomes

23rd June 2023

Wine drinking is linked to a lower risk of death from cardiovascular disease but also reduces the risk of developing both cardiovascular and coronary heart disease, according to the findings of a recent meta-analysis.

Previous studies have hinted that the polyphenolic content of wine confers a cardio-protective effect whereas consumption of spirits, increases the risk of ventricular arrhythmias. In fact, evidence points to a J-shaped relationship between wine consumption and vascular risk.

Whether these purported benefits of wine are influenced by potential confounders such as age, gender, smoking status and the duration of follow-up within studies is uncertain. For the present study published in the journal Nutrients, researchers undertook a meta-analysis to examine the association between wine consumption and cardiovascular outcomes and assessed if this association was influenced by personal and study factors. The researchers looked for studies in adults and where the reported outcomes were cardiovascular mortality, cardiovascular disease (CVD) and coronary heart disease (CHD).

Wine consumption and adverse CV outcomes

There were 25 studies with 1,443,245 subjects included in the final analysis.

Wine consumption was associated with a 24% reduced risk of CHD (relative risk, RR = 0.76, 95% CI 0.69 – 0.84). In addition, there were also significant reductions in the risk of CVD (RR = 0.83, 95% CI 0.70 – 0.98) and for cardiovascular mortality (RR = 0.73, 95% CI 0.59 – 0.90).

In a sensitivity analysis, these associations remained statistically significant. However, publication bias was evidence for the link between wine and CVD but not for either CHD or cardiovascular mortality.

In further analysis, the effects of participants’ mean age, the proportion of women in studies, the duration of follow-up or if whether individuals currently smoked, did not impact on the reported associations.

The researchers did caution that increasing wine consumption could be detrimental for patients who are vulnerable to alcohol due to age, medication or pathology. They also suggested that further research is required to differentiate the observed effects by the type of wine.

How a humble, collaborative approach can fuel advances in cardiovascular care

13th April 2023

Michael Henein is a professor of cardiology at Umeå University and Heart Centre, Sweden.

Professor Michael Henein

A consultant cardiologist in both Sweden and the UK, Michael Henein provides clinical cardiology services as well as transthoracic, stress and transoesophageal echo and carotid scanning at the Harley Street Clinic. He previously spent 15 years at the Royal Brompton Hospital as a consultant in cardiology and echocardiography having led the echocardiography department between 2001 and 2006.

To date, Professor Henein has supervised 21 PhD students at Imperial College and Umeå University and 100 MSc students between Imperial and Canterbury Christchurch University. He has also published more than 400 cardiology papers in peer-reviewed journals and edited seven textbooks.

Professor Henein is passionate about supervising international students and establishing strong academic partnerships with universities across the world. Here, he speaks to Hospital Healthcare Europe about the current projects he’s involved in.

You’ve mentored and encouraged PhD and MSc students from all over the world. What drives your passion for this collaboration?

Most of my projects are done with either my current or previous PhD students who’ve graduated. Personally, I think it’s very important to establish strong academic partnerships with international universities to help with the collaborative exchange of ideas, skills and approaches towards difficult clinical issues and research with good clinical and academic outcomes.

I’ve mostly worked with students from the UK, Sweden, Kosovo, Greece, Italy, Nigeria, Ireland, Egypt and China, all of whom have graduated and now hold important clinical and academic positions in their home countries.

There’s been significant media attention recently on elite athletes seemingly developing heart problems mid-match. What are your thoughts?

Strong evidence suggests that people who undergo frequent strenuous exercise could develop arrhythmia or heart failure. We do not have any means by which we can predict which individuals will switch from being healthy to developing problems in the future, but we know it can end in disaster.

About six years ago, we looked at the effect of regular strenuous exercise on adolescents’ heart function. I’ve suggested to Flavio D’Ascenzi, one of my former PhD students, who is currently associate professor in Siena, in Italy, that we should get that group back on a 10-year follow-up. We would test them using the same methods used before to see who remains healthy and who may have developed changes and repeat again in another 10 years. These longitude studies are very difficult to design and ascertain, but this is a very good start with quite a unique group of individuals.

You and your team are currently involved in a research project on hypertension. Can you tell us more?

Hypertension is the most common disease we see in our cardiology practice. Long-standing high blood pressure is known to affect heart structure and function. Although it can be controlled, many people develop coronary heart disease (CHD) and strokes as a result. They could be symptomatic or asymptomatic, but it needs to be properly assessed.

We’re currently looking at identifying the predictors of CHD in these patients using non-invasive investigations like dobutamine stress echocardiography. This is a well-established, non-invasive investigation for significant coronary artery disease, which has zero radiation and is very patient friendly. Now’s the time to pull all the available evidence and do a detailed meta-analysis.

You say you have a broad interest in research based on clinical questions we do not have answers for. Can you provide an example?

It’s very difficult to believe that atherosclerosis pathology chooses one branch of the aorta and doesn’t touch the rest. The scientific question here is, ‘is there any strong evidence to show that atherosclerosis disease is shared between different arterial systems?’.

In 2021, we published a paper on the results of a meta-analysis that compared the relationship between the phenotypic manifestation of coronary and carotid atherosclerosis – the two most commonly affected systems by atherosclerosis – using available imaging techniques. A total of 89 papers with 22,683 patients comparing carotid and coronary atherosclerosis were included in the analysis.

Our findings showed moderate relationship between carotid intima-media thickness and severity of coronary artery disease. Stenosis is important and not only serves in predicting the presence of severe disease but also helps in identifying patients demonstrating established arterial disease who need optimum risk factors control and follow-up management.

The results of the study supported the concept that atherosclerosis affects both carotid and coronary systems – although not always in an identical phenotypic manner. They also highlighted the benefits of examining carotid arteries whenever coronary artery disease is suspected.

You recently investigated the relationship between the presence and severity of carotid and coronary calcification in a group of patients with coronary artery disease. What did you discover?

The study was conducted on 63 patients presenting with unstable angina or positive stress test for myocardial ischaemia. All patients had CT scans of the carotid and coronary arteries using the conventional protocol and Agatston scoring system. Risk factors for atherosclerosis were also analysed for correlation with the extent of arterial calcification. In patients with coronary disease, the carotid calcification pattern appeared to be similar between the right and left systems in contrast to that of the coronary arteries. The coronary artery calcium (CAC) score correlated only modestly with the carotid score, despite being significantly higher at 10-fold. Hypertension was related to the CAC score, while diabetes and dyslipidaemia correlated with coronary calcification.

Why is a collaborative approach to working so important?

We can learn from one other. I have an interest in echocardiography, for example, but I cannot do it on my own. In Sweden Norrlands Heart Center, I had a technician who worked closely with me all the time. He updated me on new technology and the latest publications and software providers. We worked as a team and were able to look at our current practice and think, ‘why don’t we try this or that ourselves’. Myocardial deformation measurements using speckle tracking technology is an example that we developed recently. Over the years, I learned new things from this technician, who has since become a professor, and we have written many papers together.

When did you first learn about CT scanning for the heart?

It was at a heart centre in Germany in 2001/2002, many years before CT coronary scanning came to England. Back in those days, it was harder to convince anyone to start thinking about implementing them in routine practice. Now, this scanning for coronary disease is everywhere, which is wonderful, and time has changed, which is encouraging. 

If we can open our eyes to what’s happening around us in Europe and North America and see the new procedures and techniques being developed locally, and have an open-minded approach, we can – in a humble way – be ahead of the game. 

We can also be prepared for patients who are increasingly doing their own research on the internet and may catch us unaware when they come to us with questions about procedures or treatments they’ve found in operation in other countries.

Michael Henein is an advisory board member for HHE Clinical Excellence in Cardiovascular Care. He will be chairing a session entitled ‘Cardiology over 100 years’ at the event on 10 May 2023. Find out more and register for free here.

Higher ozone levels linked to increased risk of hospital admission for cardiovascular diseases

30th March 2023

Increased ozone pollution has been associated with an increased risk of hospital admission for a range of cardiovascular diseases

Higher atmospheric ozone levels have been linked to a greater risk of a hospital admission for a range of adverse cardiovascular events according to the findings of a time-series analysis by Chinese researchers.

Although there are a number of clearly recognised risk factors for cardiovascular disease, recent studies generally support positive associations of exposure to chemical environmental stressors such as air pollution, with an increased risk for cardiovascular mortality and morbidity. Moreover, some evidence points to adverse effects associated with exposure to ozone and which appears to affect several pathways associated with cardiovascular disease. In addition, other work found a statistically significant association between short-term changes in ozone and mortality for 95 large US urban communities. However, while these data link ozone with mortality, much less is known about the association between the gas and cardiovascular morbidity and for which, hospital admissions, could serve as a useful proxy.

In the current study, Chinese researchers undertook a multi-city, time-series study to explore the associations of exposure to ambient ozone with daily hospital admissions for cardiovascular diseases over a two-year period. The city-specific daily concentrations of 8-hour maximum average ozone (O3) and 24-hour average of O3 were obtained, together with data on both fine particles (PM2.5), inhaled particles (PM10), and other gases such as sulphur and nitrogen dioxide and carbon monoxide.

Ozone pollution levels and risk of hospital admissions for cardiovascular disease

During the two-year period, there were 6,444,441 hospital admissions for adverse cardiovascular events in the 70 cities included in the study.

The results showed that a 10 μg/m3 increment in the two-day average daily, 8-hour maximum ozone concentrations, was associated with an increased risk for admission of 0.46% for coronary heart disease, 0.45% for angina pectoris, 0.75% for acute myocardial infarction and 0.41% for ischaemic stroke.

In fact, the researchers also calculated the excess risk attributable to higher ozone levels and different adverse cardiovascular events. For example, that there was a 6.52% excess risk of an acute myocardial infarction (AMI) for a high O3 concentrations (≥100 μg/m3) compared to lower levels of < 70 μg/m3, which is considered to be naturally occurring level that is not due to human activity. Furthermore, the AMI risks were also elevated by 3.28% when ozone levels were ≥ 70 μg/m3 and 2.35% for levels between 70 and 99 μg/m3.

The authors concluded that ambient ozone was associated with increased risk of hospital admission for cardiovascular events and which was higher as levels of the gas increased. They added that these data should prompt the need for greater control of high ozone pollution.

Jiang Y et al. Ozone pollution and hospital admissions for cardiovascular events. Eur Heart J 2023

Herpes zoster infection linked to higher risk of stroke and coronary heart disease

9th January 2023

Infection with herpes zoster appears associated with a longer term higher risk of both a stroke and coronary heart disease

Infection with herpes zoster is associated with a higher long‐term risk of a major cardiovascular event such as a stroke and the development of coronary heart disease, according to an analysis of three large, prospective studies by researchers from Harvard Medical School, Boston, US.

Herpes zoster (HZ) occurs after reactivation of the varicella-zoster virus which is both persistent and clinically dormant, within spinal ganglia or cranial sensory nerves following an initial infection with varicella. In fact, HZ strikes millions of older adults annually worldwide and disables a substantial number of them via post-herpetic neuralgia. Moreover, in recent years, emerging evidence suggests that HZ infection leads to 1.3 to 4-fold increased risk of cerebrovascular events with a higher risk among adults under 40 years of age and within one year after an HZ episode. However, what remains unclear, is the long‐term association between HZ infection and the risk of adverse cardiovascular events or cardiovascular disease.

In the present study, US researchers investigated the longitudinal association of herpes zoster (or ‘shingles’) and the risk of stroke or coronary heart disease (CHD) among participants in 3 large US cohorts; the NHS (Nurses’ Health Study), NHS II (Nurses’ Health Study II), and HPFS (Health Professionals Follow-Up Study). Within the three cohorts, participants were asked to self-report about clinician‐diagnosed shingles and the year of diagnosis. The primary exposure for the study was categorised according to time (in years) since the participant’s HZ event and those with no history of HZ served as the reference group. The researchers then categorised the time since HZ as never, 1 to 4 years since infection, 5 to 8 years, 9 to 12 years and ≥13 years. In their analysis, adjustment were made for several factors that could potentially be related to HZ and stroke or CHD, including age, race, smoking history, body mass index, waist circumference etc.

Herpes zoster infection and cardiovascular events

The study included data on 79,658 women in the NHS, 93,932 in the NHS II and 31,440 men in the HPFS (2004-2016), without prior stroke or CHD. During >2 million person-years of follow-up, 3603 incident stroke and 8620 incident CHD cases were documented.

In a pooled analyses and compared to those without a history of HZ infection, the multivariable-adjusted hazard ratio (HR) for stroke was non-significant for those with 1 to 4 years since HZ infection (HR = 1.05, 95% CI 0.88 – 1.25). However, the associations became significant as the duration from infection increased. For example, among those with 5 to 8 years since HZ, the hazard ratio was 1.38 (95% CI 1.10 – 1.74) and 1.28 (95% CI 1.03 – 1.59) among those with for 9 to 12 years since HZ. Interestingly, the association became non-significant among those with ≥13 years since HZ (HR = 1.19, 95% CI 0.90 – 1.56).

When considering CHD,  the corresponding multivariable-adjusted hazard ratios were similar, e.g. 1.25 (95% CI 1.07 – 1.46) for 9 to 12 years and, as with stroke, the risk of CHD became non-significant after ≥13 years (HR = 1.00, 95% CI 0.83 – 1.21).

The authors concluded that herpes zoster is associated with a higher long-term risk of a major cardiovascular event, underscoring the importance of prevention of infection.

Curhan SG et al. Herpes Zoster and Long-Term Risk of Cardiovascular Disease. J Am Heart Assoc. 2022

HDL cholesterol protective role questioned

2nd December 2022

Increased HDL cholesterol is considered protective against CVD but a study in Black and White individuals has re-examined this role

HDL cholesterol is generally considered to be protective against coronary heart disease (CHD) but a recent analysis that included both Black and White patients suggests that higher levels offer no protection in either race with an elevated CHD risk due to low levels only relevant for White individuals.

Globally, coronary heart diseases were estimated to kill 17.9 million people in 2019, which represents 32% of all global deaths, with 85% of deaths due to heart attack and stroke. Since the early 1970’s, there has been a well-established and inverse relationship between plasma high-density lipoprotein (HDL) cholesterol and CHD risk. However, whether this relationship remains for different ethnicities is uncertain. It is known for example, that after accounting for social determinants of health and other risk factors, Black patients have a similar risk of a fatal CHD to White patients, but that the risk for a nonfatal CHD is consistently lower for Black people. The underlying reasons behind this difference are unclear and have been further confounded by the somewhat paradoxical observation that low levels of HDL cholesterol are associated with a reduced risk of incident CHD in black participants.

In trying to better understand the relationship between HDL cholesterol and incident CHD, a team of US researchers turned to data collected in the REasons for Geographic And Racial Differences in Stroke (REGARDS) Study, designed to examine underlying racial and regional differences in stroke and mortality. The researchers selected a cohort without baseline CHD and for whom a wide range of clinical and demographic factors were collected. The cohort was followed over time and the number of incident CHD (i.e., definite or probable nonfatal myocardial infarction or CHD death) were recorded.

HDL cholesterol and CHD events in Black and White patients

A total of 23,901 participants with a mean age of 64.1 years (58.3% female) and of whom, 57.7% self-identified as White were included in the analysis and followed for a median of 10.7 years. During the follow-up there were 1,615 CHD events of which 41.1% occurred in Black participants and 45.5% in women.

When analysing the relationship between CHD events and plasma LDL cholesterol in fully adjusted models, for every 1 standard deviation increase in LDL levels, there was a modest increase in CHD risk (Hazard ratio, HR = 1.10, 95% CI 1.05 – 1.17). Similarly, for triglyceride levels, there was also a modest increase in CHD risk (HR = 1.05, 95% CI 1.01 – 1.10). However, in fully adjusted models, there was a non-significant association between HDL cholesterol (HDL-C) levels and CHD risk (HR = 0.95, 95% CI 0.89 – 1.02).

But when researchers examined the relationship between HDL-C and CHD risk stratified by race, they found something unusual. As might be expected based on the currently known relationship, a low HDL-C level was associated with an increased risk of CHD, but this was only significant for White patients (HR = 1.22, 95% CI 1.05 – 1.43). Among Black patients the relationship was not significant (HR = 0.94, 95% CI 0.78 – 1.14). Furthermore, a high HDL-C level was not protective in either White (HR = 0.96, 95% CI 0.79 – 1.16) or Black (HR = 0.91, 95% CI 0.74 – 1.12) patients.

Based on these findings, the authors concluded that current high-density lipoprotein cholesterol–based risk calculations could lead to inaccurate risk assessment in Black adults.

Zakai NA et al. Race-Dependent Association of High-Density Lipoprotein Cholesterol Levels With Incident Coronary Artery Disease. J Am Coll Cardiol 2022

Study suggests thyroid cancer increases coronary heart disease risk

10th November 2022

Having thyroid cancer is linked to a higher risk of coronary heart disease and which persists in those under 65 years for at least 5 years

Patients with thyroid cancer (TC) have a greater risk of developing coronary heart disease and in those under 65 years of age, this elevated risk persists for at least five years after their cancer diagnosis according to an observational study by Taiwanese researchers.

In 2020, the global estimated rate of thyroid cancer was 10·1 per 100 000 women and 3·1 per 100 000 men, although mortality rates were lower at 0·5 per 100 000 and 0·3 per 100 000 for women and men respectively. Surgery is the mainstay of treatment in nearly every case of thyroid cancer although radiotherapy can also be used. If the thyroid is removed, then patients will require life-long therapy with levothyroxine both to replace the hormone and lower the risk of cancer recurrence. However, long-term use of levothyroxine may cause marked impairment of cardiac functional reserve and physical exercise capacity. Whether these changes increase the subsequent risk of cardiovascular disease remains uncertain with some evidence that such patients have a higher incidence of cardiovascular disease morbidity. In contrast however, other work has shown that the incidence of cerebrovascular disease, cerebral infarction, ischaemic heart disease, ischaemic heart attack and heart failure are no different between those with TC and the general population.

With some uncertainty over the relationship between TC and the risk of cardiovascular diseases, in the current study, the Taiwanese researchers turned to data contained within a nationwide population-based cohort to retrospectively examine this relationship. They chose a baseline date for their analysis as the time when TC patients underwent a thyroidectomy but excluded those aged < 20 and > 85 years and anyone with a history of coronary heart disease (CHD) or atrial fibrillation. They set the primary endpoint of interest as hospitalisation for CHD defined in terms of fatal and non-fatal CHD. Secondary outcomes included ischaemic stroke (IS) that required hospitalisation and atrial fibrillation, which again required hospitalisation. The researchers calculated a standardised incidence ratio (SIR) as the ratio of observed to expected CHD cases, stratified by age and gender within the general population.

Thyroid cancer and risk of coronary heart disease

A total of 4,274 individuals who had thyroid cancer without CHD and a mean age of 49 years (24.4% male) were included in the analysis and followed-up for a mean of 3.5 years.

During follow-up, there were 69 CHD events in those with TC and the SIR was significantly higher than expected in the age-standardised population (SIR = 1.57, 95% CI 1.2 – 1.93). However, the rate of IS was not significantly different (SIR = 0.74, 95% CI 0.47 – 1), neither was the incidence of cardiovascular disease (SIR = 0.88, 95% CI 0.70 – 1.05) or atrial fibrillation (SIR = 0.74, 95% CI 0.42 – 1.06).

When researchers considered the SIR over time, particularly among those under 65 years of age, the elevated risk remained significant, 5 years after the date of their TC diagnosis (SIR = 2.08, 95% CI 1.5 – 2.66) although it was non-significant among those over 65 years of age (SIR = 1.0, 95% CI 0.57 – 1.42).

The authors concluded that thyroid cancer patients had a greater risk of CHD than the general population without the cancer and that this risk persisted for at least 5 years. They called for future research to further investigate this observed association.

Tsai MC et al. Association between thyroid cancer and cardiovascular disease risk: a nationwide observation study. Sci Rep 2022

All-cause mortality risk reduced by maintenance of physical activity in CHD

17th June 2022

All-cause mortality can be significantly reduced among patients with coronary heart disease who maintain physically active over time

Patients with coronary heart disease (CHD) who continue to be physically active over time and even those who reduce their activity, have a significantly lower risk of all-cause mortality compared to those who remain physically inactive.

This was the key finding from a meta-analysis by a team of researchers from Switzerland and Colombia.

Cardiovascular diseases are the leading cause of mortality around the world with an estimated 17.9 million deaths in 2019 and which represented 32% of all global deaths. One modifiable risk factor for cardiovascular disease (CVD) is physical activity and in a 2017 study found that a higher level of recreational and non-recreational physical activity was associated with a lower risk of all-cause mortality and CVD events.

However, whilst there are clear benefits from increased levels of physical activity with respect to all-cause mortality among those with CHD, what is less clear, is the impact of changes in physical activity over time.

For the present study, the researchers performed a systematic review and meta-analysis to examine the association between longitudinal trajectories of physical activity and both all-cause mortality and cardiovascular disease mortality in those with CHD.

The team included studies with a longitudinal design in adults with CHD and which provided data on all-cause and CVD mortality.

For the purposes of the analysis, the researchers examined the changes in all-cause mortality by different levels of reported physical activity trajectories. For example, those who remained inactive, those who increased their physical activity and finally individuals who decreased their activity level over time.

For the analysis, hazard ratios were calculated and regression models were adjusted for age, gender, ethnicity, smoking status, alcohol intake and co-morbidities. All of the studies assessed physical activity using validated questionnaires.

All-cause mortality and physical activity trajectories

A total of 9 articles were included in the final analysis, all of which were prospective in nature with 33,576 patients with an overall mean age of 62.5 years and the proportion of women ranging from 18 to 56%.

Compared to those who remained inactive over time, the risk of all-cause mortality was 50% lower among those who remained active (hazard ratio, HR = 0.50, 95% CI 0.39 – 0.63), 45% lower for those who increased their level of activity (HR = 0.55, 95% CI 0.44 – 0.70).

Moreover, even among those who had been active but who became less active, there was still a 20% lower all-cause mortality risk (HR = 0.80, 95% CI 0.64 – 0.99).

These reductions in risk were similar for cardiovascular mortality. For example, it was 51% lower for those who remained active (vs inactive) however, it became non-significant for those whose activity levels had reduced over time (HR = 0.91, 95% CI 0.67 – 1.24).

The authors concluded that there was a possible protective mortality benefit of either increased or continued activity among patients with CHD and suggested that physical activity trajectories should be considered in clinical practice.

Gonzalez-Jaramillo N et al. Systematic Review of Physical Activity Trajectories and Mortality in Patients With Coronary Artery Disease J Am Col Cardiol 2022

Should saturated fat be back on the menu?

15th July 2020

The 1950s diet-heart hypothesis linked saturated fat to the development of coronary heart disease. But does more recent evidence suggest otherwise? Rod Tucker finds out more.

Developed during the 1950s, the diet-heart hypothesis suggested that greater consumption of fat raised cholesterol levels and led to the development of coronary heart disease (CHD). As such, the recommendation to reduce consumption of fat, particularly saturated fat was subsequently adopted by the select committee on nutrition and human needs1 and incorporated into international nutritional guidelines.

Fast forward to 2017, and the American Heart Association concluded in an advisory paper that ‘lowering intake of saturated fat and replacing it with unsaturated fat, especially polyunsaturated fats, will lower the incidence of CVD’.2 In the UK, advice from the NHS suggests that eating ‘too much saturated fats… will raise “bad” LDL cholesterol in your blood’.3

While now a cornerstone of dietary advice as a means to minimise the risk of developing CHD, closer inspection of the literature on the relationship between saturated fat and heart disease reveals that there is little objective evidence to support this premise. So, is it time to stop vilifying saturated fat and dispense with years of dietary dogma that has created a fear of fats and advocated that we embrace ‘low fat’ foods?

Saturated fat and heart disease

The relationship between intake of saturated fats and heart disease has been extensively explored in studies including more than 75,000 people and in recent years, reviews have failed to find convincing evidence for its harmful effects. For example, a systematic review and meta-analysis in 2015 which included data from 12 prospective studies concluded that intake of saturated fat is not associated with all-cause mortality, cardiovascular disease, coronary heart disease, ischaemic stroke or type 2 diabetes.4

However, cohort studies lack vigour and more robust evidence from randomised trials is required to more clearly define this relationship. In the late 1960s, the Minnesota Coronary Experiment (MCE), a randomised trial in over 9,000 people, was designed to test whether replacement of saturated fat with vegetable oil rich in linoleic acid reduced heart disease.

The study was conducted within state mental health hospitals and a nursing home to allow for a tight control of diet. Over a period of 4.5 years, researchers compared two diets containing either 18% saturated fat (the control diet) and 9% (the intervention diet). When reported, the authors found no difference in cardiovascular events, cardiovascular deaths or even total mortality.5

The study was not published until 1989, but in 2015, researchers uncovered further and unreported data from the MCE study and re-analysed the data. They concluded that while reducing saturated fat did reduce serum cholesterol by up to 13%, this was not associated with any benefit in terms of either myocardial infarction or mortality.6

Further evidence that saturated fats have no real effect on CHD comes from a 2020 Cochrane systematic review. This found that reducing saturated fat had little or no effect on cardiovascular mortality, all-cause mortality, non-fatal myocardial infarction or CHD mortality.7 In contrast to the recent reviews, earlier analyses have reported beneficial effects in terms of CHD events from replacing saturated fat with polyunsaturated fatty acids.8

Other recent data even suggests that a higher intake of carbohydrate (as recommended in dietary guidelines) increases the risk of heart disease. In the prospective urban rural epidemiological (PURE) study which included 125,287 participants from 18 countries who were followed for 10 years, it was found that replacing saturated fat with carbohydrate had an adverse effect on blood lipids.

As the authors concluded, ‘high carbohydrate intake has the most adverse impact on cardiovascular disease risk factors, whereas monounsaturated fatty acids seem to be beneficial and saturated fatty acids are not harmful’.9 In a further analysis of total mortality and major cardiovascular events, the same group reported that ‘higher saturated fat intake was associated with a lower risk of stroke’.10

Although saturated fat is known to increase low density lipoprotein (LDL) cholesterol levels, LDL itself actually comprises several sub fractions of differing size. The smaller and more dense LDL particles are associated with a higher CHD risk11 than the larger LDL particles and studies suggest that saturated fat increases the concentration of larger LDL particles.12 In addition, saturated fats increase high density lipoprotein levels (HDL) which are considered to be protective against heart disease.13

In summary, although saturated fats have been demonised over the years with a cultural shift towards eating low fat foods, this does not mean that saturated fat is without harm. In a recent study of 195,658 participants followed for 10 years, it was found that saturated fat intake was significantly associated with all-cause mortality but only where it represented 20% or more of total calorie intake.14

An unintended consequence of the shift to low fat foods, has been the recommendation to limit many foods including dairy products, eggs, unprocessed meats, all of which have been shown to reduce the risk of CHD.15 Individuals should therefore not seek to avoid eating these healthy foods simply because of a fear that they contain saturated fat.


  1. Dietary goals for the United States. United States. Congress. Senate. Select Committee on Nutrition and Human Needs. Washington: U.S. Govt. Print. Off, 1977:92.
  2. Sacks FM et al. American Heart Association. Dietary fats and cardiovascular disease: A Presidential advisory from the American Heart Association. Circulation 2017;136(3):e1-e23
  3. NHS. Fat: the facts.
  4. De Souza RJ et al. Intake of saturated and trans unsaturated fatty acids and risk of all-cause mortality, cardiovascular disease and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ 2015;351:h3978
  5. Frantz ID et al. Test of effect of lipid lowering by diet on cardiovascular disease risk. The Minnesota Coronary Survey. Arteriosclerosis 1989;9(1):129–35
  6. Ramsden CE et al. Re-evaluation of the traditional diet- heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968–73). BMJ 2016;353:i1246.
  7. Hooper L et al. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev 2020;5:CD011737.
  8. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomised controlled trials. PLoS Med 2010:7(3):e1000252.
  9. Mente A et al. Association of dietary nutrients with blood lipids and blood pressure in 18 countries: a cross-sectional analysis from the PURE study. Lancet Diabetes Endocrinol 2017;5:774–87.
  10. Dehghan M et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet 2017;390:2050–62.
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