‘Milestone' treatment could reshape future leukaemia care
A UK trial has found that a chemotherapy-free approach to treatment may lead to better outcomes for some leukaemia patients, in what scientists are calling a "milestone".
The groundbreaking UK-wide trial could reshape the way the most common form of leukaemia in adults is treated.
Researchers from Leeds assessed whether two targeted cancer drugs could perform better than standard chemotherapy among patients with chronic lymphocytic leukaemia (CLL).
Chronic lymphocytic leukaemia is the most common form of leukaemia in adults, with about 4,000 new cases recorded in the UK every year.
The Flair trial, which took place at 96 cancer centres across the UK, saw 786 people with previously untreated CLL randomly assigned to receive standard chemotherapy; a single targeted drug, ibrutinib, or two targeted drugs taken together, ibrutinib and venetoclax, with treatment guided by personalised blood tests.
Researchers found that after five years, 94 per cent of patients who received ibrutinib plus venetoclax were alive with no disease progression.
This compares with 79 per cent for those on ibrutinib alone and 58 per cent for those on standard chemotherapy, according to the study, which has been published in the New England Journal of Medicine and presented to the European Haematology Association congress in Milan, Italy.
Meanwhile, 66 per cent of patients on the new combination had no detectable cancer in their bone marrow after two years, compared with none of the people who received ibrutinib alone and 48 per cent on chemotherapy.
Ibrutinib is a type of drug known as a cancer growth blocker, which works by stopping signals that cancer cells use to divide and grow, and venetoclax blocks the functions of a protein found in CLL cells.
Experts said that the new treatment regime was also tolerated better than traditional treatments.
Dr Talha Munir, consultant haematologist at Leeds Teaching Hospitals NHS Trust, who led the study, said the Flair trial is a 'milestone'.
'We have shown that a chemotherapy-free approach can be not only more effective but also more tolerable for patients,' she said.
'By tailoring individualised treatment based on how well the cancer responds, we're moving into an era of truly personalised medicine.'
Catherine Whitfield, 63, from Farnley, West Yorkshire, was diagnosed with CLL in 2018 after she noticed symptoms including bleeding gums, constant illness and neck pain.
She signed up for the trial, which was coordinated by the Leeds Cancer Research UK Clinical Trials Unit at the University of Leeds and sponsored by the University of Leeds.
'After three years of treatment, I am still MRD negative – that means no cancer cells,' she said.
'I lost my husband to cancer. I have seen how hard it could be.
'My first thought after my diagnosis was, I will never see my grandchildren being born and growing up.
'Now I have two grandchildren, Drew and Alaia, and they are a delight and highlight the joys of a healthy life'.
Ms Whitfield added: 'The way this trial was explained, it just made sense. Also, the thought of chemotherapy was scary to me. The trial felt right. And it was.'
Many people who have chronic lymphocytic leukaemia do not have any symptoms, but the main ones include:
swollen glands, usually in your neck or under your arms
losing weight
getting ill a lot
feeling tired even though you've had a good night's sleep
a rash that looks like small bruises or bleeding under the skin and does not fade when you roll a glass over it, similar to meningitis
bleeding or bruising for no reason
looking unusually pale and feeling breathless
a high temperature even though you're not unwell
aches and pains that will not go away
sweating at night
Dr Iain Foulkes, executive director of research and innovation at Cancer Research UK, which funded the trial along with AbbVie, and Johnson and Johnson, said: 'The results of the Flair trial show that we can provide kinder, more targeted treatment for chronic lymphocytic leukaemia, which gives people with CLL more precious time with their loved ones.
'We're hopeful that the results of the Flair trial will power new treatment options for leukaemia and other blood cancers, thanks to the efforts of researchers at in Leeds and across the UK working together on this trial.'
Hashtags

Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Yahoo
an hour ago
- Yahoo
The assisted dying debate has been politics – but not as we know it
The House of Commons is a place defined by confrontation where political battles play out and engage more actively with their constituents. But the atmosphere could not have been more different on Friday, as those on both sides of the assisted dying debate listened respectfully, almost solemnly, to one another in the final hours before . As MPs headed for the division lobbies, the bill's supporters seemed confident but nervous. Read more: When the voting was completed and the result imminent, a long and profound silence fell over the House. From the press gallery, it seemed that the entire Commons was holding its breath together, collectively aware of the historic moment we were all about to witness, whatever the outcome. The woman at the centre of this seismic moment, the bill's sponsor Kim Leadbeater, braced herself as the result came in. Many months of pressure and responsibility appeared to be lifted from her shoulders as the win was announced and colleagues gathered to commend her efforts. Throughout the process this been politics but not as we know it, with party divisions put aside and MPs asked to search their own consciences and come to their own conclusions. It has created a more collaborative atmosphere in parliament and encouraged MPs to engage more actively with their constituents. In the end there was still anger, frustration and disappointment among those who were against the law change, either on principle or because they believed the legislation was flawed. And of course, politics will go back to being combative and voices in the Commons will be raised once again. But for a brief period, historic change was calmly ushered in. The challenge for the proponents now is to take the legislation through the next phases and deliver it with the same smoothness and determination.


Medscape
3 hours ago
- Medscape
Jun 20 2025 This Week in Cardiology
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending June 20, 2025, John Mandrola, MD, comments on the following topics: a big, deep dive into CTA and fractional flow reserve CT, and a sobering report on the new EVOQUE valve. Mark Petrie from the UK writes to correct my description of the CRAAFT-HF trial. I mistakenly said it was a surgical vs catheter ablation trial, but Dr Petrie said that they were actually randomizing to atrial fibrillation (AF) ablation plus heart failure with reduced ejection fraction (HFrEF) medical therapy vs HFrEF medical therapy alone in patients with left ventricular dysfunction. Saturday is the first day of summer. Where has the time gone? There is a spot at the halfway point of our 5 AM ride, about 20 miles out in the country that the sun rises over a farm on a hill. It's a hot spot on the ride but once a year I try to convince the crew to stop for a photo. Imaging and Behavior Change Five Reasons I Don't Believe an Imaging Test Improves Outcomes My friends in Edinburgh, who have been leaders in the use of coronary computed tomographic angiography (CCTA), report on a nested substudy within the SCOT-HEART 2 trial. Let's start with SCOT-HEART 1, which randomized symptomatic patients (stable CP) to receive CTA plus standard care vs standard care alone — which often included functional stress testing. CCTA-led care led to a significantly lower rate of death from cardiovascular (CV) death and nonfatal myocardial infarction (2.3 vs 3.9%). This seemed like a big win for CCTA, but the controversy centered on the fact that the small delta in statin use in the two groups (more in the CTA) was nowhere near enough to drive the large reduction in myocardial infarction (MI). For instance, I cited Andrew Foy, who calculated that to believe statin therapy drove SCOT-HEART, you'd have to believe statins have a number needed to treat (NNT) of 3, not its normal 50-100. Nonetheless, the use of CCTA is different in cost-constrained systems like Scotland. In Scotland, it is used to reduce coronary angiography and PCI. Knowledge of coronary artery disease (CAD) is used to guide medical therapy, and there is no incentive to do more angiography. In the United States, CCTA is used as a cash machine, because the nanosecond an American patient and American doctor see CAD, the patient gets a hotline to the cath lab and PCI. The problem, of course, with anatomical testing is that you can have twinge of chest pain from a cramp and if you have incidental CAD, boom, you now have lifelong dependence on antiplatelet. Now to the SCOT-HEART 2 trial, which is a randomized controlled trial (RCT) using CTA. The study question is this: Is screening with CTA more clinically effective than CV risk scoring with an equation? The plan is to enroll at least 6000 people (not patients, people ) in Scotland who are at risk of heart disease to CTA-guided management vs equation-guided management. They will use an equation called ASSIGN, which is like the pooled cohort equation (it only uses outcome data from Scotland) and includes the social deprivation score. Those in the equation (or standard care) arm get lifestyle advice and lipid-lowering therapy (LLT) for 10-year risk > 10%. Those in the CTA arm get lifestyle advice for normal CTA, lifestyle advice, plus LLT and aspiring for non-obstructive disease, and for those with obstructive disease, they get lifestyle advice, LLT, aspirin, ACE inhibitor plus review by a cardiologist. At 5 years, the primary outcome is coronary death or MI. There are lots of secondary outcomes. JAMA Cardiology has published a nested cohort study within SCOT-HEART 2 looking at a primary outcome of the proportion of participants who achieved the National Institute for Health and Care Excellence (NICE) recommendations for diet, BMI, smoking and exercise. Diet, smoking and exercise were self-reported, and weight, BMI, and step count were measured. The study population included 400 people enrolled over 4 years, which does not seem like a lot. At 6 months, those in the CTA screening were more likely to meet the primary composite endpoint of compliance with the NICE recommendations for diet, BMI, smoking and exercise — it was 17% vs 6%. These seem low but that's because people had to reach all four of the components. The relative risk increase was an odds ratio of 3.4 times more likely to achieve these four goals in the CTA group. Other secondary findings were that fewer participants in the CTA group were recommended for LLT (51% vs 75%). That's because the risk score placed more above 10% but with normal CTA, LLT was not given. Even though fewer LLTs were recommended with CTA, acceptance of LLT was higher in the CTA group, 77% vs 46%. In the end, statistically similar numbers of patients took LLT in both groups (44% vs 35%). Antiplatelet use was much higher in the CTA group, 40% vs 0.5%. The authors broke down secondary outcomes based on whether CTA showed disease, and this associated with slightly lower weight, BMI, waist circumference, blood pressure, total and LDL cholesterol concentrations, and greater improvements in daily step count. Another interesting twist was that 100 individuals in the CTA arm were given a verbal report of their CTA and the 100 were shown their images. No differences were seen in the two subgroups for the primary and secondary outcomes. The authors were pretty calm in their conclusions. They note these interesting observations, that CTA resulted in more accurate risk stratification where some patients with high equation risk had no disease and some patients with low equation risk had disease. CTA did increase acceptance of lipid-lowering therapy as well as increase the proportion of patients reaching lifestyle goals. The obvious take-home message here is that this data supports the seeing-is-believing idea. The editorialists wrote enthusiastically that: 'the results of this nested randomized clinical trial within the SCOT-HEART 2 study are striking. A preventive strategy incorporating CCTA appeared to be not only more precise but also more motivating to participants and clinicians. CCTA reclassified 1 in 3 individuals based on 10-year risk score, targeting therapy to those who were assumed to derive greatest benefit.' I laud the Edinburgh team for doing SCOT-HEART 2. But the differences in verbal acceptance of lifestyle, or LLT use, or aspirin use, or tiny blood pressure (BP) changes are not what we care about. The only outcome is MI or coronary death. When you submit a person with no disease to medical imaging, it ought not be for motivation. It should only be for their health benefit. The changes in lifestyle or drug use or more precise risk stratification are made up surrogate endpoints that have meaning only if there is a difference in outcomes. I strongly oppose the use of imaging to scare patients into taking statins or not eating chips. In Scotland, the downstream effects of CTA may be different than in the US. Here, it is highly likely that seeing disease will affect future interventions. Let's say there is mild disease noted on a screening CTA. Maybe the US patient is given statins and aspirin. Well, what do you think happens in the months or years to come the next time that patient has a twinge of CP? It's right to the ER and then the cath lab for stents or bypass. We need to celebrate the fact that SCOT-HEART 2 will be done, but until then, we need to resist the urge to image our patients based on minor differences in surrogate endpoints, some of which are self-reported. Heart disease treatment and prevention is simple: it's lifestyle (including diet and exercise), possibly lipid-lowering therapy. Imaging is not required and should not be done until there is evidence it improves outcomes. Symptoms Don't Always Indicate the Severity of Coronary Artery Disease JACC-CV Interventions has published a research letter looking at the association between cardiac symptoms and coronary plaque. I will call this a back-to-the-future study with modern imaging confirming a lesson that Dr Bernard Lown described a half-century ago Only now we get to toss around terms like fractional flow reserve, total plaque atheroma, and — sit down for this one — artificial intelligence–enabled quantitative coronary plaque analysis (AI-QCPA) tools. I will speak about the letter, which is modest, but the main thing that happened is that it caused me to look into the FFR-CT data. And OMG. The researchers used data from the ADVANCE registry, which was a 5000-patient registry from multiple centers done to assess how often FFR-CT changes management vs regular CT. The sample included about 4300 patients who referred for coronary CT and had a coronary lesion. Symptoms were characterized by a) squeezing chest or neck pain, b) pain precipitated by exertion, c) relieved by nitrates or rest. Typical angina had all three; atypical angina had 2 of 3, noncardiac had one, and there was also a group with dyspnea only. There were five groups of patients: 25% no symptoms 10% dyspnea only 6% noncardiac 37% atypical chest pain 22% typical angina Now pause. The authors had total plaque volume and FFR-CT on each of these patients. Then they just did correlations. And they found, with these correlations: Only typical angina had a positive correlation with plaque atheroma. Typical angina also correlated strongly with negative values of FFR-CT. The authors also noted, surprisingly, that atypical chest pain, noncardiac chest pain, and dyspnea each correlated with higher FFR-CT, greater than 0.8 suggestive of normal flow. The authors and imaging proponents seem excited about this. In a Medscape news article, one of the authors says: 'Even having no symptoms was not a reliable indicator of cardiovascular health in these patients. Just because a patient doesn't report any symptoms doesn't mean there is no atherosclerosis.' Also quoted in the news article, Matthew Budoff, MD, a cardiologist at UCLA said: 'cardiologists rely heavily on symptoms to determine how severe cardiovascular disease is, but the new research is beginning to dispel that idea.' Budoff also added that: 'the new findings support the idea CT angiography should be a bigger part of the diagnostic process, so clinicians can look not only at whether a patient has stenosis but also go beyond to see if they have any atherosclerosis or plaque that might be a target for medical therapy.' This letter seems so funny to me. One of the first lessons we were taught at Indiana University in the 1990s was that when a patient presented with typical angina and even a positive stress test, that catheterization would show left main or severe triple vessel disease about 10%, it would be normal in 10%, and somewhere in between in 80%. In other words, symptoms are a very unreliable marker of CAD. Now we have a study that uses have artificial intelligence (AI), CT, FFR, and multivariable regression to confirm something that's as old as the hills. I don't agree with Dr Budoff that cardiologists rely heavily on symptoms. At least not in many places in the US. The main requirement for a stress test in the US is insurance coverage and the main requirement for a cath is a wrist. We don't rely on symptoms. We rely on imaging and angiography. I have this saying that I don't say too much anymore but think often: If every stress imaging machine broke for a month, heart disease outcomes would not change. I wonder whether this also applies to CTA imaging and surely to FFR-CT. A colleague tells me that FFR-CT adds $1500 to basic CTA. I find that shocking. Now I want to go to the advance registry paper in 2018. The main value in this research letter was a kick in the butt to go back to the original evidence for this FFR-CT business, the publication of the ADVANCE registry in the European Heart Journal in 2018. First author Fairbairn. This will be a trigger warning because this is one of those things you can't unsee or unhear. ADVANCE registry included about 5000 patients with symptoms concerning for CAD and atherosclerosis on CCTA. The authors recorded the basic info, symptoms, CCTA and FFR-CT findings were recorded along with treatment plans. They also had 90-day outcomes. For each enrolled patient, a clinical management review committee used data from coronary CTA to determine the management plan using the following criteria: (a) optimal medical therapy, (b) percutaneous coronary intervention (PCI), (c) coronary artery bypass graft surgery (CABG), or (d) more information required. The primary endpoint of the registry is the reclassification rate between the management plan based on coronary CTA alone vs CTA plus FFR-CT. Two teams came up with the original plan based only on CTA. A site team and a blinded core team from Duke. The primary endpoint was the reclassification of the treatment plan from the CT-FFR results. The primary results were that it changed management in about two-thirds of the cases. It was hard for me to see a pattern in the reclassification. The authors tell us later that the majority of subjects were safely deferred to medical management alone, and only a minority required 'further testing.' A second finding was that rate of no significant disease at angiography was significantly lower in patients who had a positive FFR < 0.8 (about 15%) vs > 0.8 (44%). Odds ratio for no significant disease was 0.19 for a positive FFR (that is < 0.8) A third finding was that 19 MACE events happened in the 90 days after the study, 10 of them were death, and all happened in the FFR < 0.8 category — 19 vs 0. The authors concluded that FFR-CT was great. It guided management, helped predict no disease, and even had a strong association with MACE events. They noted this: 'FFR-CT led to a recommendation of invasive coronary angiography (ICA) in only 40% of subjects in a cohort with an anatomic obstructive disease rate of 72%, and subjects referred for ICA downstream were significantly more likely to have obstructive disease at ICA if they had a positive FFR-CT.' And this: 'Importantly, a negative FFR-CT was associated with an excellent short-term prognosis, as none of the 1600 subjects with negative FFR-CT experienced death, MI, or unplanned hospitalization for ACS and urgent revascularization.' A colleague in imaging advises me that this was one of the major studies cited to establish FFR-CT. My gosh, this is terrible. What a mess. First of all, the study was sponsored by HeartFlow. It was a late-breaker at ESC in 2018. I must have had jet lag because I missed it. Much of my criticism follows a Twitter thread from my friend Venk Murthy at University of Michigan. A primary endpoint in change in management in a voluntary registry sponsored by the company is about as weak an endpoint as you can get. Why isn't this a measurement of clinical psychology? What if you chose, say, in a non-industry-funded study, a doctor team skeptical of FFR-CT. I bet few would be swayed by the CT-FFR results. Another problem was that most of the FFR-CT values were abnormal in the left anterior descending artery (LAD) and were between 0.7-0.85. We know this from the IQR values. But now I will cite a study from Christopher Cook in Darrell Francis' group published in JAMA Cardiology 2017. What this London group found is that when doing a systematic review of all studies measuring the diagnostic accuracy of FFR-CT, they found that values just under the cutoff of 0.8 (that is, between 0.7 and 0.8) had the lowest accuracy — only 46% accurate. Pause there. That's like a coin flip. Cook et al report that if you want accuracy from FFR-CT, say 82% overall accuracy threshold, you needed values lower than 0.63 or above 0.83. And if you wanted more stringent 95% and 98% diagnostic accuracy thresholds from FFR-CT, you needed values lower than 0.53 or above 0.93, and lower than 0.47 or above 0.99, respectively. A third issue is that most of the patients (77%) were nontypical angina — either atypical or non-cardiac pain. But we know from the Manesh Patel seminal NEJM paper from 2010 that when patients with atypical symptoms go to cath, the chance of obstructive disease is low — regardless of the results of stress testing. In fact, a positive stress test only changed the likelihood of having CAD from 35% to 41%; hence, my stance that if every stress imaging machine broke, CV outcomes would hardly change. The point in citing this seminal paper is that most patients in the ADVANCE registry study — the 77% with atypical symptoms — should not have had a change in management. A fourth issue is that the MACE events are 100% noise — 19 vs 0. And 10 deaths in the first 90 days. I can't even believe they mentioned MACE events. The CI for the odds ratio goes from 1.2 to 326. The P-value, however, was calculated to be significant at .039, which is crazy. So, in sum, this is one of the weakest, late-breaking, practicing-changing trials I have seen. It's a psychology experiment and we have no idea a) which treatment strategy was best, and b) what meaning is there in changing a treatment strategy without knowing which one is correct. If we wanted to know about FFR-CT, it's simple: you randomize people to care with the HeartFlow FFR-CT vs those without. Then you measure outcomes — MI, CV deaths, even urgent revascularization. But this was not done. Instead, FDA approves the HeartFlow, proponents and key opinion leaders speak highly of it, these studies are not highly criticized, and CT scans get $1500 added to them. HeartFlow was approved de novo in 2014 but received a 2019 clearance for 'virtual modeling.' When I asked my AI friend Claude to explain the difference between the two designations — 2014 and 2019 — one of the 'significant' points was a business model expansion wherein the original FFR-CT was a one-time diagnostic test, but the 'planner (the virtual modeling) creates additional revenue opportunities for each patient who needs intervention.' And then this: the 2019 decision Expands HeartFlow's market from diagnosis into treatment planning. My AI program Claude must not know I am a critical appraiser because it then wrote: Physicians can now use HeartFlow for the entire patient journey: diagnosis → treatment planning → post-intervention assessment. This creates much stronger physician adoption and stickiness. And it makes the cost–benefit analysis more favorable since one CT scan can support multiple clinical decisions. The 2019 Planner approval was huge for HeartFlow because it transformed them from a diagnostic company into a comprehensive coronary care platform. Instead of just answering "Does this patient need a catheterization?", they can now answer: "Exactly how should we treat this patient's disease?" This is why HeartFlow's valuation and market penetration accelerated significantly after 2019. They weren't just competing with stress tests anymore; they were competing with the entire invasive workup process. I had no idea this stuff was happening. What a tragic waste of money. This may be one of the lowest value medical interventions I have seen. And you think I am wrong to be hopeful about FDA new leadership. Regulators should have required an RCT. Since they did not require and RCT, physicians should. Companies are not nefarious. They simply jump over the bar we hold for them. In this case the bar was ridiculously low. Speaking about lax FDA regulation, JACC has published a sobering research letter on the transcatheter tricuspid valve replacement called the EVOQUE valve. This one is also really scary. On this I hardly need commentary; I can just tell you the data. First author was Lior Lupu. FDA approved the valve in February 2024. This was based on the pivotal TRISCEND II trial, which was driven quality-of-life measures, not hard outcomes, and was not blinded. Thus, placebo effects were surely present. The group of authors from Washington, DC used the MAUDE database at FDA, which stands for Manufacturer and User Facility Device Experience. It contains information about device malfunctions, injuries, and deaths associated with medical devices that have been reported by manufacturers, healthcare facilities, and users. The main weakness of MAUDE is that there is no denominator and it's voluntary. In the year since approval, the research team found 150 reports on EVOQUE that describe 158 events. 1. Bradycardia or high degree atrioventricular (AV) block was most common (n = 70 or 44%) and there were 2 deaths. 66 of the 70 required pacemakers. Most were detected at the implant however a third were seen later between days 3 and 90. 2. Device malposition, migration, or embolization occurred in 33 patients (20.9%), causing 6 deaths. Most events were diagnosed within 3 months: 76% intraprocedurally, 14% within 2 days, and 7% between 3 days and 3 months. Management included transcatheter valve-in-valve implantation in 10 cases (eg, SAPIEN-in-Evoque), with 2 requiring a second valve for optimization. Two patients underwent transcatheter treatment for paravalvular leak, while 16 required surgery. 3. EVOQUE leaflet thickening or thrombus was identified in 20 patients (12.7%), with clinical or hemodynamic consequences reported in 16 of the 20. Cases were detected within the first month (56.3%), between months 2 and 6 (25.1%), and after 1 year (18.8%). Management included thrombolysis (n = 4), transcatheter valve-in-valve implantation (n = 2; 1 also had device migration), and surgery (1 patient with severe postprocedural thrombosis with hemodynamic instability). 4. Cardiac tamponade was reported in 8 patients (5.1%), with 5 patients undergoing surgery and 4 deaths. 5. Venous injury or bleeding occurred in 8 patients (5.1%), with 2 deaths. 6. Five cases of ventricular tachycardia, fibrillation, or cardiac arrest were reported: 2 intraprocedurally and 3 postprocedurally (days 0, 4, and 7). 7. Mechanical failure of the delivery catheter was reported in 4 patients (2.5%), all due to nose cone separation. The authors write that while bradycardia, tamponade, valve injury, and valve thrombosis had been reported in the trial, valve malposition, migration, or embolization — the second most frequently reported adverse event in this research letter — were not reported in the trial. So, they were new discoveries. Also, additionally, 3 cases of ventricular arrhythmia or cardiac arrest were reported within the first postprocedural week without a definite etiology. Nose cone separation wherein the nose can go missing into the PA also occurred. Like I said, I hardly need comment because the list of complications is so sobering. Of course, MAUDE has no denominator, but on the other hand it is also voluntary, so this is likely underreporting. I would note that only 237 patients received a valve in the TRISCEND II pivotal trial. There were substantial complications noted. To me, this was quite lax regulation. First, there should have been a trial with a sham procedure. Quality-of-life metrics are meaningless when one group gets a procedure and the other group gets bland white tablets. Second, there should have been more patients in the trial. And third, the approval should have been contingent on a required database, such as that with TAVR. This report is really scary given the number of deaths. In fact, mortality from tricuspid valve surgery is the main reason transcatheter techniques were designed. In the transcript, I highlighted in orange font the number of deaths. I counted 14 deaths and 5 cases of ventricular tachycardia/cardiac arrest. Proponents may cite the learning curve, but I doubt it because I read that the company did a slow rollout where centers who were part of the trial were first. And you wonder why I am a medical conservative and slow adopter.

Vogue
5 hours ago
- Vogue
I Drank Beet Juice Every Day for a Month—It Had This Unexpected Effect
Disclaimer: I am a caffeine fiend. I drink so much coffee that my local barista regularly chides me, reminding me 'it's not good for your heart' to start the day with a triple-shot flat white before 6 a.m. But when I became pregnant—and had to limit my daily caffeine intake to around 200 mg a day (or two single-shot coffees)—it was a struggle to say the least. Pre-pregnancy, I also indulged in nootropics, Diet Coke, and caffeine-infused anything to help me get through the day. But now? It was all a no. And I was flat out tired. That's when I stumbled upon a juice called the 'Fatigue Fighter' made of beets, apples, oranges, celery, and ginger. I was willing to give basically anything a try, and quickly downed an entire container. Delicious. But it wasn't until my energy soared that I became a believer. Read on for all the reasons that maybe you should give it a try, too. What are the benefits of drinking beet juice? I've waxed lyrical about my personal experience with beet juice, but what are the actual health benefits? Evelina Sabonaityte, MD and clinical nutritionist, claims that beet juice is 'a nutrient-packed elixir.' Here are some of the benefits of beet juice, according to Evelina and Dr Katy Kasraie, one of the general practitioners at The London General Practice.