Latest news with #cardiology
Yahoo
8 hours ago
- General
- Yahoo
'Meant to be': Oklahoma cardiologist treats man's heart attack symptoms mid-flight
An Oklahoma cardiologist had a full circle moment when a Dutch man complained of chest pains on their shared flight. Dr. TJ Trad, a cardiologist at Stillwater Medical Center and founder of the nonprofit Cura for the World Foundation, was traveling home from a medical mission trip in Uganda when he was awoken on the flight to Amsterdam, CNN reported. A man was complaining of chest pain and needed a doctor, he was told by a nurse on his team. Trad found the man drenched in sweat, and he asked the doctor, "Am I going to die?" "Not today," Trad told him before getting to work. Trad had the medications needed to treat a heart attack on hand — including nitroglycerin, Aspirin, Plavix, metoprolol and lisinopril — part of the around two dozen medications he carries with him on medical mission in case anyone on his team has an emergency. But Trad, 43, also had a pocket-sized electrocardiogram, which he carries with him since having his own heart scare last year. One February morning in 2024, just days before he was scheduled to fly to Uganda for a planned medical mission trip, Trad said he was doing a procedure on a patient when he began having chest pain. He was experiencing an 80% blockage in one of his arteries — he had a stent placed that same day and canceled his trip to Uganda. As a way to mark the one year anniversary of his cardiac scare, Trad finished the climb to Everest Base Camp at the beginning of March. "I believe that everything happens for a reason, as cliche as that might sound," Trad said. "Maybe the event that occurred a year ago was the nidus for me to be on that specific plane to help that specific person. Every time, let's say something negative or positive happens, it's good to kind of sit back and reflect on what's the downstream effect of that? So yeah, I feel like we were meant to be on that flight to help." Not only does Trad believe he was meant to be on the flight to help the Dutch man, but he has the same sense regarding the trip to Uganda. While on their trip, Trad met an 8-month-old girl with a 7.8 millimeter ventricular septal defect. The funds have already been raised to cover her heart surgery, which should be taking place soon, he said. "What are the chances that a cardiologist would appear at that specific time in her life ... it's one of those things," Trad said. "It's not a coincidence." The man on the plane told Trad his chest pain, on a scale of 1 to 10, was a 10. It was a pain Trad had warned his patients about, but also one he had felt himself. About 15 minutes after Trad gave him medication, the man's chest pain was gone. But the doctor and nurse continually monitored his symptoms, checking his heart rhythm every five to 10 minutes for the duration of the flight. "After his symptoms subsided, I told the pilot, 'We bought time to get to Amsterdam so that he can go to the hospital there,'" Trad said. CNN reported that the man was examined for 12 hours at the hospital and was not diagnosed with a heart attack, stroke or pulmonary embolism — possibly as a result of Trad's treatment of the patient. Before going their separate ways, the man's wife told Trad, "You're our angel in the sky." This article originally appeared on Oklahoman: Oklahoma doctor treats heart attack symptoms on flight home from Uganda
Yahoo
8 hours ago
- Business
- Yahoo
A cardiologist overhauled his diet to boost his longevity. Here's the grocery store path he takes to stick to his meal plan and avoid bad foods.
Ultra-processed foods are consistently linked to bad health outcomes, but they can be hard to avoid. A cardiologist writing a book about longevity decided to quit UPFs almost entirely. He shops the perimeter of the grocery store and enjoys more salads and yogurt. When cardiologist Eric Topol goes to the grocery store these days, his cart stands out among the crowd. It's no longer filled with boxes or packaged goods, he says it's largely just fresh produce — a big change from what he used to buy. "I was reading a lot of labels, and now I avoid things with labels," Topol told Business Insider. "When I'm in the grocery store and I'm only buying produce, people look at me like, 'what's wrong with this guy?'" It all happened about a year ago, as he was deep into research for his new bestselling book "Super Agers: An evidence-based approach to longevity." That's when he overhauled his relationship with packaged and mass-produced foods, cracking down on any ultra-processed food (UPF). "I call 'em UFOs," Topol said. "A lot of those things I didn't realize were so full of bad things." Topol shops now using the common nutritional rule-of-thumb to stick to the perimeter of the grocery store, the area where the fresh fruits, vegetables, nuts, bulk grains, and frozen veggies are stored. It's those middle aisles full of ultra-processed products that he generally avoids. As Topol explains in his new book, ultra-processed foods are "the polar opposite" of fiber, a key nutrient abundant in fresh foods like fruits, vegetables, nuts, beans, and grains, which we know is great for our long-term health in all different kinds of ways. For example, fiber slows down and aids digestion, improves cholesterol, fosters the health of the gut microbiome, and even helps stabilize blood sugar. UPFs generally don't. "What is referred to as the 'Western diet,' rich in ultra-processed foods, is pro-inflammatory and linked with metabolic dysfunction, cardiovascular disease, diabetes, and colon cancer," Topol's book says. His diet wasn't wildly unhealthy before, but he's become a more rigorous shopper as a result of his latest research. "If it's packaged or boxed or canned, I know it's probably gonna be a problem," Topol said. "I'll check it out. Sometimes, you can be surprised." Ultra-processed food researchers say not all UPFs are equally unhealthy. Studies show that whole grain breakfast cereals and ultra-processed yogurts aren't as bad for you as hot dogs, packaged desserts, or sugar-sweetened drinks like soda and juice. That second group of foods is more consistently linked to poor long-term health outcomes, like higher rates of type 2 diabetes and heart disease. Some cans and boxes in the grocery store aren't even ultraprocessed at all. A can of chickpeas or some black beans seasoned with salt, frozen vegetables, canned fish — these are simply processed foods. They aren't linked to all the same bad health outcomes as UPFs, instead, they're great shortcuts to help encourage more healthy eating at home. Topol says his new shopping routine has morphed his daily diet in a near-effortless way. Plus, he doesn't have to spend so much time reading labels anymore, looking for the long list of ingredients he tries to avoid like high-fructose corn syrup, palm oil, artificial sweeteners, and more. "I eat salad at night, I eat yogurt and some berries in the morning, and not a whole lot in between," he said. "It's a pretty healthy diet, I think." Read the original article on Business Insider


Medscape
a day ago
- Health
- Medscape
May 30 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 May 30, 2025, John Mandrola, MD, comments on the following topics: listener feedback, CRT vs CSP, important clues on the ECG, beta-blocker interruption after myocardial infarction, novel approaches to LDL-C lowering, and ICD decisions in cardiac sarcoidosis. Dr Steve Dickson, a heart failure cardiologist from Kansas City, writes via email to push back on my skepticism about rapid initiation of guideline-directed medical therapy (GDMT) in heart failure (HF). Dr Dickson says I am right about the STRONG-HF trial, which used cardiologists for the majority of follow-up visits. And while cardiologist-led care may currently be the case in many clinics across the country, he writes, times are changing. Hospitalists, primary care practitioners (PCPs), and advanced practice practitioners are becoming more comfortable with these life-saving medication classes. The future of heart failure care isn't just the burden of cardiologists, but internal medicine where there are more reinforcements. Dr Dickson says that in his clinic they run a '4 Weeks 4 Meds' program for patients with heart failure with reduced ejection fraction (HFrEF), mainly through nurse practitioners that he guides and manages. He says it's 'quite aggressive but I can assure you my CEO loves seeing his readmissions drop.' My comment to this is that I fully support programs like '4 weeks 4 meds' programs. It's a great idea, but of course, it takes administrative support, incentives. And, I would add that this is a great use of advanced practice clinicians. I say congratulations and I hope more programs like this become a reality. Clearly, HF care would improve if it did. The obvious advantage of such a program is not only getting more patients on max GDMT but also avoiding harm from overzealous GDMT titration. Cardiac Resynchronization Therapy vs Conduction System Pacing – CONSYST-CRT As many of you know, because I have said it so many times, the most exciting thing in EP right now is not ablation but pacing, specifically, conduction system pacing (CSP). I saw a Tweet this week, saying that ablation has become more anatomic and rote, and pacing is becoming more physiologic. It used to be the opposite. In an ablation, we would map and study electrophysiology, and in pacing we would simply flop a catheter in the right ventricle (RV) and we would just screw it in wherever it fell into the RV. Now in ablation we put in a pulsed field ablation (PFA) catheter and boom. E-grams are gone. PFA ablation is ruining EP. Now, during a pacemaker we meticulously record and pace in areas of the conduction system. 6+ years ago, we were doing it with the His bundle, and now it's the left bundle. To do CSP is to bathe yourself in beautiful physiology. But beautiful images of CSP on an ECG are not evidence. What we need is evidence that it is superior to biventricular (BiV) pacing for the treatment of patients with heart failure and left bundle branch block (LBBB). The thing is, in BiV pacing, we have strong evidence, from multiple trials, that biV pacing reduces hard outcomes, like mortality, compared to standard RV implantable cardioverter defibrillators (ICDs) or medical therapy. We think, emphasis on think, that because CSP narrows the QRS, and some smaller studies have shown improved hemodynamics with CSP, it is similar to, or superior to, BiV pacing. We need trials. Well, I am a local principal investigator here at my hospital for the US government-funded Left vs Left trial, which will have death and hospitalization for heart failure (HHF) as a primary endpoint. Planned enrollment is 2100 patients and follow-up is for 5 years. That's a long time to wait. This month, JACC EP has published another attempt to compare CSP to BiV pacing in CRT-eligible patients. Spanish investigators have now published the CONSYST-CRT trial. This was a randomized controlled trial (RCT) of just 134 patients of CSP vs BiV pacing. The design was non-inferiority of CSP. The primary endpoint was a composite of many things: death, transplant, HHF, or a left ventricular ejection fraction (LVEF) improvement of less than 5% at only 12 months. I hope you are seeing the problems: I will go over the issues in the comments. First finding: 18 of 67 patients crossed over from CSP to BiV pacing. Second finding: 23.9% in the CSP group had a primary outcome event vs 29.8% of the BiV pacing. The absolute risk difference was –5.9%. The confidence interval went from –21.2%, which is far better with CSP, to 9.2% worse for CSP. The accepted non-inferiority margin was 10% worse, and so 9% is less than 10% and this allowed a claim of non-inferiority with a P value of .02. Secondary endpoints also favored CSP. QRS narrowing was better in the CSP arm. Echo response was better, as was a NYHA functional class improvement. The combined endpoint of death, transplant, and HHF also showed non-inferiority, though I could not find confidence intervals on the difference. The authors concluded: CSP was non-inferior to biV pacing in achieving clinical and echocardiographic response, suggesting that CSP could be an alternative to biV pacing. I laud trials and clinicians who attempt them. CSP vs biV pacing is an important question. But if you are going to experiment on people, you need to have a chance of telling a difference. There is no way this trial had a chance with only 134 patients—1 in three who crossed over—to detect signal from noise. There were 16 vs 20 primary outcome events, respectively. There were 1 vs 3 deaths, 0 vs 1 transplant, and 8 vs 10 HHF. The most common outcome was failing to improve an ejection fraction (EF), which is far from a hard clinical outcome. That is a tiny number of events. Not only was the composite endpoint problematic, but follow-up for a year is totally inadequate. Left vs Left is asking the same question and enrolling 2000 patients — almost 20 times more patients. It would have been fine to compare hemodynamics, but we have oodles of these studies showing similar effects on EF with CSP. I mean no malice to the Spanish team, and to be sure, I was part of the His-SYNC trial, another woefully underpowered trial, but this type of effort tells us little to nothing about the long-term effects of the two strategies. Underpowered trials, I think, should be avoided. Since the beauty of the ECG is what got me interested in cardiology, I am always on the lookout for studies on the ECG. A UCSF group reports a research letter in Circulation EP on the association between a fragmented QRS and myocardial fibrosis burden and autopsy-defined arrhythmic causes among presumed sudden cardiac death (SCD). QRS complexes should be sharp and narrow. There should be no notches or fragments. This is a report from the ongoing project called the POST SCD or 'Postmortem Systematic Investigation of Sudden Cardiac Death' study. The idea is to use autopsy and clinical data to adjudicate arrhythmic (potentially treatable with an ICD) vs nonarrhythmic death (overdose, pulmonary embolism, stroke, etc). So far, the team has had 943 presumed SCD, of which 402 had ECGs before death. And 98 (or about 1 in 4) of these had histogical data. Fragmented QRS was defined as greater than 1 notch for QRS <120 milliseconds (ms) and >2 notches if the QRS ≥120 ms and fragmented QRS's had to be in 2 leads. The findings of this research letter were: Presumed SCD with a fractionated QRS on more than 1 lead were more likely to have arrhythmic causes compared with presumed SCDs without fractionated QRS 76% versus 55%; odds ratio, 2.6 [95% CI, 1.11–6.5]; P = .036, No other ECG marker was associated with higher odds of arrhythmic death. Coronary artery disease (CAD) was the most common cause of fractionated QRS. Presumed SCDs with fractionated QRS in greater than 1 lead had higher mean total and replacement fibrosis as well as more interstitial fibrosis burden than presumed SCDs without fractionated QRS ( P < .05 for all). I cover this imperfect study because the value of the ECG is under-recognized. I say imperfect because only half the presumed SCD had ECGs before death; and only a fraction of these had histological samples. What's more, the difference in associations were statistically significant but the positive and negative predictive value of fractionated QRS is surely low. But I want to consider this a public service announcement to my colleagues in cardiology. When you are sorting out whether a patient (say with syncope or near syncope) has a worrisome structural heart condition, study the QRS. When someone is telling me the story of syncope, my first question after the story is what does the QRS look like? Fragmented QRS is an electrical manifestation of disordered ventricular conduction, which is often due to scar, and disordered conduction, aka, anisotropy, sets the stage for reentry. Recall one of the fundamentals of cardiology: reentry requires three things: two pathways, delayed conduction, and unidirectional block. Scar sets the stage because there all three possible. In the same way that atrial structural disease increases the odds that a PAC fibrillates the atria, ventricular structural disease makes it more likely that a PVC fibrillates the ventricle. No, I am not saying that every notched fragmented QRS is malignant, but it's a clue, it's one piece of data. Don't overreact, but don't ignore the QRS. EHJ has a substudy from the French ABYSS trial of beta-blocker (BB) interruption vs continuation after myocardial infarction (MI). The substudy purported to show 'spikes' in HR and blood pressure (BP) after BB discontinuation. And this explains why the ABYSS study failed to show that stopping beta-blocker therapy could be safely done in stable post-MI patients. None of this is correct. None. And I want to correct the record about ABYSS, again. In my mind, ABYSS is entirely consistent with the REDUCE-AMI trial of not using BB in the post-MI patient. REDUCE-AMI found that not giving long-term BB resulted in similar major adverse cardiovascular events (MACE) outcomes compared with standard BB in post-MI patients with a normal EF. The main ABYSS trial, published in NEJM in August 2024, compared interruption of BB or continuation of BB in patients who had a previous MI and EF > 40% and MI at least 6 months before randomization. The median time from MI to randomization was just about 3 years. ABYSS enrolled about 3700 patients. It had a non-inferiority (NI) design with a 4-point composite endpoint of MI, stroke, death, or hospitalization for cardiac reason. The NI margin was a difference of 3% points for the upper bound of the 95% CI. The results were that interruption was not only not non-inferior to continuation but actually inferior to continuation. The numbers: 23.8% primary outcome events in the interruption group vs 21.1% primary outcome events in the continuation group Absolute risk increase of 2.8% with 95% CI that went from 0.1 to 5.5. Since 5.5% was greater than the NI margin of 3%, NI was not met. And when you looked at the CI, the entire 95% CI was above 0 for the interruption group so it was actually inferior. But, But. The entire composite was driven by hospitalization for cardiac reasons — 349 vs 307. There were no differences in death, no difference in MI, and no difference in stroke. The major MACE outcomes were nearly identical. The only reason ABYSS found to be against interruption was a surrogate outcome requiring adjudication of hospitalization. The less biased outcomes of death, stroke, and MI were identical. Now to the EHJ substudy, which looked at changes in BP and HR from baseline to post-randomization in the two groups. They also assessed the changes in HR and BP impact on the primary endpoint for the prespecified subgroups of patients with or without history of hypertension. With little to no surprise the BB interruption group sustained an increase in heart rate (about 10 bpm) and systolic blood pressure (SBP) (3.7 mmHg). These deltas remained stable after discontinuation over months. With regard to the hypertension (HTN) and no-HTN groups which were almost 50-50 split, there were largely similar effects. That was an increase in heart rate and SBP. Also not surprising was that the primary outcome occurred more often in patients with HTN than those without HTN, showing that HTN patients are higher risk. I am not sure we needed that analysis because HTN is a known risk factor. The observed harm (higher rate of the primary outcome) was numerically higher in the HTN group; the difference was not statistically significant. In other words, there was no evidence of a heterogenous treatment effect for HTN or no HTN. But remember, 'harm' as described by the primary outcome in ABYSS is flawed because it was driven only CV hospitalizations. In Table 2, the authors show the results of the components of the primary outcome in the BB interruption and continuation arm based on the subgroup of HTN — and in MI, stroke, and death, the P values for interactions were close to 1, as in absolutely no difference. The authors concluded: Interruption of beta-blocker treatment after an uncomplicated MI led to a sustained increase in BP and HR, with potentially deleterious effects on outcomes, especially in patients with history of hypertension. My friends, the ABYSS trial was a perfectly nice trial. It addressed an important question. The problem was the choice of endpoint. When you look at MI, stroke, and death, BB interruption was totally fine. This substudy showing why ABYSS found harm is flawed because the main trial chose a flawed endpoint. Further, finding that HR and BP go up slightly when a BB is stopped is like finding out you get wet when walking in the rain. BB reduce HR and BP. When you stop them, HR and BP go up a bit. Since the main trial found no increase in MACE, we can say that that small rise in HR and BP don't have deleterious effects. The most we can take from this study is that there does not seem to be a heterogenous treatment effect for the presence of HTN. I think we can stop BB in patients with a history of MI if they have normal EF and no other reason to take BB. The one caveat to my argument that death, MI, and stroke were not different was that it was a little underpowered. For the composite of death, MI, and stroke, the hazard ratio was 0.96 in the interruption vs continuation arm, but the confidence interval went from 0.74 to 1.24. So, interruption could be 26% better or 24% worse than continuation. And perhaps that is why the authors decided to add CV hospitalizations. Yet when you combine the data from REDUCE-AMI and recent observational data from Denmark, the ABYSS finding of no increase in MACE after BB interruption supports the idea that interruption of BB after MI is reasonable and safe. And, of course, less medicine is better. Is Lifelong LDL-C Lowering Within Reach? The heart-1 Gene-Editing Trial Heart-1 Gene Therapy Trial Pauses Enrollment JACC has published a phase 2 dose-ranging study with another oral PCSK9 inhibitor, called AZD0780. In other words, it doesn't have a name yet. The drug has a novel mechanism, which I won't delve into at this point, but it did achieve a dose-dependent drop in LDL cholesterol (LDL-C). The max dose of 30 mg achieved a 50% placebo-adjusted reduction of LDL-C and all patients were on statins but had LDL-C > 70 mg/dL. No adverse effects were noted but the study was quite short at only 12 weeks. The accompanying editorial was quite good. I learned a lot from it. First, there are multiple oral PCSK9 inhibitors in development. I think this is a good thing because pills are better than shots. I say that because shots increase the work of being a patient. There is just more inertia and insurance restrictions and effort required to take a shot, however infrequently. The editorialists also discussed the pricing dilemma and the role of pharmacy benefit managers (PBM) whose rebate-based pricing models often dictate drug availability. To be honest, I don't quite understand PBMs well enough to explain them, but I can say that I don't get the feeling they contribute much to the health of US citizens. There is also a potential — and I emphasize the potential part — for permanent inhibition of the PCSK9 complex via CRISPR/Cas9-mediated gene editing. Dr Sekar Kathiresan's company Verve Therapeutics is working on that, and it has progressed to early-stage human trials. The one-and-done approach to LDL-C management is obviously a high reward, high risk strategy and there will need to be rigorous safety data before this could become a reality. Two safety issues have arisen: one a patient developed very high hepatic enzymes, and in another trial, two patients had serious cardiac events — not felt to be due to the intervention. So we shall see. There would have to be a heck of lot more data on safety before I signed up to permanently change my genes — especially when you can accomplish the same thing with a tiny daily pill. I know that I sound old saying this, but if you stop and think, it's quite shocking that such an approach could be close to becoming a possibility. Editing genes so as to reduce LDL-C, for life. Wow. One of the toughest calls in EP is deciding on ICD treatment of patients with suspected cardiac sarcoid. It's hard for many reasons, not least because the diagnosis of cardiac sarcoid, and its risk stratification is difficult. European Heart Journal has published a nice study from a Dutch center and two American centers. They had about 1500 patients with biopsy proven sarcoid, mostly non-cardiac who had not had ventricular tachycardia (VT) and therefore were being considered only for a primary prevention ICD. They then compared outcomes based on multiple ways to risk stratify. I, for instance, did not know that there were multiple professional societal recommendations for an ICD. There is the 2014 Heart Rhythm Society (HRS) statement, the 2017 AHA/ACC guideline and the 2022 European Society of Cardiology (ESC) guideline. And they're all a little different. The purpose of this study is that Dutch and American authors propose is that cardiovascular magnetic resonance imaging (CMR) phenotyping is better. CMR phenotyping sounded tricky but it they made it seem easy. You are either CMR high or low risk. It's based on EF and 'pathology frequent LGE'. There were four CMR phenotypes: (1) no late gadolinium enhancement (LGE) and normal LVEF, (2) no LGE and abnormal LVEF, (3) pathology-frequent LGE, and (4) pathology-rare LGE. Pathology-frequent LGE included at least one of four features: sub-epicardial, multifocal, septal, and right ventricular free wall involvement. They then dichotomized CMR phenotypes into high-risk (pathology-frequent LGE) and low-risk (no LGE and normal LVEF, no LGE and abnormal LVEF, or pathology-rare LGE) phenotypes. The next step was to follow the 1500 or so patients over 5-10 years for VT events. Of note, most were young, average age 54 years. Let me stop there and say when you have a 50-something year old with heart block, before putting in a pacemaker, stop and think about sarcoid. Do a CMR first. The first finding was that when an ICD was indicated based on either the society or CMR phenotype the likelihood of a ventricular arrhythmia (VA) event at 10 years was high. Ranging from 20% to 35% for the high risk CMR group. When an ICD was not indicated by either the society recommendations or CMR phenotype, the rates of VA were low, but ranged from 5% in the HRS statement to 2.6% for CMR low risk. They key findings were seen in Figure 3: the CMR dichotomized method had the best are under the curve (AUC). At 5 years, it was 0.86 for VT events. That's pretty darn good, and statistically better than each of the professional society criteria for ICD. The problem of course is that the ICD need is imperfect. A subgroup of the 1500, about 8% or 119 patients received a loop recorder. About a third had high risk CMR and two thirds had CMR low risk. 4 of 38 patients (or 4% per year) had VT in the CMR high risk 1 of 81 patients in the CMR low-risk had a VA for a 0.4% per year risk. This illustrates the problem of prediction: most high-risk patients do not have a VT event and not every low-risk patient remains free of VT. As it is ischemic and non-ischemic HF patients. I do like the CMR approach, though. And this study is quite nice, as there were more than 1000 patients, all with biopsy-proven sarcoid, good follow-up, and centrally adjudicated blinded CMR. There were — as always — limitations. ICD therapy as a VT event is not always a surrogate for SCD. Just because a person has VT therapy (shock or anti-tachycardia pacing) does not mean it was aborted SCD. Second, patients without ICDs in this study may have had VT and it went undetected. To me, if we had some replication or confirmation of such a simple CMR high- or low-risk strategy, it would seem best. Realizing of course the imperfect nature of prediction of VA events. The things to keep in mind with ICD therapy is that a) it is not an insurance policy; insurance policies confer no risk to the policy holder, and ICDs surely do; b) you always want to deploy an ICD in a patient with a high-risk of the primary outcome (the VA) and a low-risk of competing risks, such as severe HF, or dementia or chronic kidney disease, or a host of disease seen in the elderly. The 54-year-old patient with heart block and LGE and reduced EF seems like an ideal patient for an ICD.


Bloomberg
a day ago
- Health
- Bloomberg
An Architectural Masterpiece in Jackson Hole Hits the Market for $60 Million
As a child growing up in Brooklyn, New York, Gerald Dorros says he was obsessed with the American West and wanted to be a cowboy. Instead, he studied medicine and become a trailblazing cardiologist who patented medical devices and was among the first doctors in the US to do coronary angioplasties. Still, Dorros loved the wide open spaces of Wyoming, and he'd often come the popular ski resort area of Jackson Hole on family vacations. In 1997 the doctor bought a tract of land in Wilson, a 20-minute drive from the town of Jackson, and built a home there. He lived out his cowboy dreams by learning to ride horses and even won a rodeo championship. But in December 2017 his home burned down in a blaze that took the fire department several days to put out. Dorros' entire family, including his grandchildren, were visiting for the holidays, but thankfully no one was hurt.


Irish Times
3 days ago
- Health
- Irish Times
Using fitness technology to improve life and health spans: ‘To be above average later in life, you need to be above average now'
High levels of aerobic fitness are the best predictor of longevity, according to cardiologist Dr Paddy Barrett, who has attracted an international following for his expertise in prevention of heart disease . Feeling how puffed you are after running up two flights of stairs might be a clue to how you are faring on that front. But a more insightful and scientific approach is to measure your VO₂ max. This is the maximum rate at which your body can transport and use oxygen to fuel muscles, expressed in millilitres of oxygen consumed per minute per kilo of body weight. 'The higher your VO₂ max, the longer you are likely to live and the less likely you are to develop the major chronic diseases of heart disease, cancer and dementia early in life,' says Dr Barrett, a specialist in heart disease prevention and cardiovascular risk management at Blackrock Health in Dublin and author of Heart: An Owner's Guide (Dorling Kindersley, 2024). No wonder then that there is growing interest in this key 'metric' for the probability of enjoying a longer lifespan and, perhaps more crucially, an extended healthspan, ie well enough to enjoy an independent and active life. Of course, the proverbial bus, literal or metaphorical, can still come along to confound any such expectation, but it is an important indicator of odds. READ MORE More than half the Irish population have a smartwatch on their wrists and many will be familiar with at least the option of using it to get a VO₂ reading. But these are estimates conjured up by algorithms based on the device's measurement of pace and heart rate, with no breath analysis involved. Some brands are regarded as better than others in their fine tuning of those algorithms for accuracy Long before the development of consumer wearable trackers, American doctor Kenneth Cooper devised a test for the US military in the 1960s to measure aerobic fitness. This is still popular today as a self-test for VO₂ max. It involves measuring how far you can run in 12 minutes and putting that figure into an online Cooper test calculator. The result can be used to look at how your VO₂ max compares within the range for your gender and age group. However, the only way to get an accurate VO₂ reading is to take a test wearing a mask connected to a machine that assesses the body's oxygen consumption while gentle movement is ramped up to full exertion. A process that was once confined to elite sports circles and research labs is becoming increasingly available to anyone interested in learning more about their fitness. Some corporate workplaces now organise on-site testing as a perk for employees. Seán Kinane came across VO₂ max testing when he was working in a gym in Perth, Australia , in 2009. Two years later, he set up Health Matters based in a gym in Tallaght , Dublin, working with athletes from a variety of sports. But he has seen demand grow 'exponentially' in recent times. 'We're doing nearly more tests in a week now than we did in a year,' he says of both VO₂ and resting metabolic rate testing, with work in corporate care having taken off in the last few years. He attributes this to people generally being more aware of health and fitness post Covid, and also to the influence of global guru Dr Peter Attia, 'beating the drum from America about the longevity aspects of VO₂'. [ How to be happy as you grow older: 'Get out and keep going' Opens in new window ] The link to longevity is very much the focus of siblings Elizabeth and Daniel O'Mahony, who this month opened AgeLess in South Dublin to offer testing for VO₂ max and/or resting metabolic rate. (The latter calculates the number of daily calories an individual needs to function while at rest and is used as a tool in weight management, be that to lose, gain or maintain.) 'We're not saying that we're going to increase people's lifespans or make people live to 100,' says Daniel, sitting with his sister in a pristine office suite in Sandyford's South Beacon Quarter. But they are confident that their 'gold standard' equipment here can give people very useful data for longevity and working towards fitness goals, be that to run a first marathon or still be able to play a round of golf at 85. Test results, he explains, can help predict what decade physical activities are likely to start to become difficult for an individual if they continue on their current health trajectory. An individual's VO₂ max typically declines by up to 10 per cent for every decade after the age of 25 to 30 but exercise helps counter the extent and impact of that decrease. AgeLess is a significant change of direction for the O'Mahonys who were both involved in the family property business for about 20 years. They were looking for an opportunity to strike out on their own and share their passion for health and wellbeing, sharpened by the experience of the Covid pandemic Daniel, who is 39 and a former smoker, says that, like many millennials, he did not think about long-term health in his 20s. But then he became an avid runner and participates in ultra endurance events. He finished 72nd in the 2021 Marathon des Sables, a gruelling seven-day race covering 250km in the Moroccan desert, and now has his sights set on next year's Ultra Trail Mont Blanc, a 117km run around the mountain involving an elevation gain of 10,000m. [ Do we really need 10,000 steps a day to stay healthy? Opens in new window ] Daniel and Elizabeth O'Mahony Elizabeth, who is 44 and a mother of two children, aged seven and four, has only taken up running recently. Motherhood, particularly having her second child during the Covid pandemic, made her more aware of her own health and the importance of physical activity for the whole family. 'For me just being able to get out and have a run in the evening or at the weekend is great for the soul. I wouldn't be doing ultra marathons or anything like that, but I've signed up now for the Women's Mini Marathon on the 1st of June,' she says. So what is involved in this test to find out how well your heart and lungs deliver oxygen to muscles? At AgeLess, there is the choice of doing it on a treadmill or exercise bike – or on your own bike fixed on a stand. For those using the treadmill, the speed and incline is gradually increased as their respiratory exchange rate (RER) is measured through the use of mask and tubing connected to a monitor, for the VO₂ max calculation. At initial walking pace, the RER will read 0.8, indicating that the person is using fat as their primary fuel source. 'As they get to a higher level of output on their exercise,' says Daniel, 'they switch over into carbohydrates as their main fuel source and the RER will have gone from 0.8 up to 1.0 and then when it hits 1.1 for anyone, that's considered a maximum effort.' At that point all the necessary data has been captured and while more competitive clients may persevere for a bit longer, others will indicate they can do no more with a thumbs down or by hitting the stop button. 'The test itself normally lasts between 12 and 15 minutes and the last three minutes are probably the hardest for people because that's when they're actually getting to their threshold,' says Elizabeth. Non-runners can opt to do a walking test using steeper inclines on the treadmill. The information readouts, which include tracking of heart rate, calories burned through the exercise test and speed of heart rate recovery, are then put in context for the client. The VO₂ max score is only part of somebody's fitness story. But once they know their baseline, the next thing to be thinking about is how to increase that. Dr Paddy Barrett, a specialist in heart disease prevention and cardiovascular risk management at Blackrock Health Dr Barrett's advice is: 'If you want to be above average later in life, you need to be above average now. Falling into the 'average' range for your age and sex is not good enough. You need to be above average at a minimum, but ideally in the top 25 per cent.' AgeLess is partnering with personal trainers, nutritionists and physiotherapists to work with clients seeking detailed, professional advice on how to act on what their VO₂ max result is telling them. They may want to look at improving their lean muscle mass and their nutrition. If clients choose to have their resting metabolic rate (RMR) measured as well, or come in just for that, the test involves simply sitting on a sofa connected to a monitor for 20 minutes. Both tests, as part of a 'longevity bundle', cost €150. Individually, the fee for VO₂ max analysis is €110 and €80 for RMR analysis. 'Having a good, lean muscle mass with a high VO₂ max is the ideal place to be,' says Daniel, who stresses that small, compound behavioural changes add up over time. 'What we would ideally like to do is get our clients, over the years, up into that 75th percentile; to have everyone aiming for what is quite an achievable percentile to be in.' Ciaran Burke of The Performance Lab ( in Clonmel, Co Tipperary, has also seen a surge of interest in knowing and tracking this fitness marker. A strength and conditioning coach who became an exercise physiologist six years ago, Burke was mainly providing testing to athletic and triathlon clubs at the outset but now goes into mainstream gyms. With rising participation in Hyrox and other forms of hybrid fitness training, people 'are just trying to find the little percentages that the athletic world, or the endurance world, already knows about', Burke suggests. 'My guiding principle is to make sure they know how to inject what they've learned into their training.' While the majority of his work is still sports performance related, Burke notes that there are also people in their 60s and 70s coming to him to get a VO₂ test 'just to sort of get a handle on what's going on'. VO₂ max testing is becoming more popular for tracking health and life spans After a baseline test to inform somebody's fitness training, noticeable change should be achievable within 12 to 15 weeks if they are following their programme correctly, he says. But he finds people are 'shocking' at judging intensity of training. The rough guide for increasing VO₂ max is that just 20 per cent of training should be high intensity for that individual, while the rest is slow, steady effort. A person's VO₂ max is not the be all and end all, explains Kinane. An athlete with a lower level could outperform a fellow competitor with a higher VO₂ max because they train smarter. It is a number that 'doesn't guarantee performance, it guarantees potential,' is how he likes to put it. 'It's learning about how to use that through training zones and energy systems and fuelling. And that's where the metabolic analysis then complements the VO₂ stuff.' Elite athletes apart, dietitian Sarah Keogh of Eat Well is a bit dubious about the value for the average person of knowing the very precise number of daily calories their body needs just to function. In her work, RMR is occasionally used for somebody, say, being tube fed in an intensive care unit. Dietitian Sarah Keogh. However, she acknowledges that for some people this number can be very motivating in calculating and sticking to an eating plan. Her main concern is where it might increase food anxiety and rigidity over daily consumption, to the detriment of good mental health and a social life.