Lance Stroll pulls out of today's race
The win saw Piastri's lead over McLaren teammate Lando Norris in the drivers' championship standings grow to 10 points Getty Images Getty Images
Lance Stroll will not compete in the Spanish Grand Prix because of 'pain in his hand and wrist, which his medical consultant believes is in relation to the procedure he underwent in 2023', Aston Martin announced late Saturday evening.
According to the team, the 26-year-old has been suffering for six weeks, and Stroll 'will undergo a procedure to rectify these issues before focusing on his recovery'. The 2023 incident referenced is a cycling accident that required surgery.
No one can replace the Canadian driver because they did not compete in qualifying. Stroll qualified P14, while teammate Fernando Alonso is set to line up 10th for tomorrow's Spanish GP.
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Lance Stroll out of Spanish GP, to undergo procedure after hand and wrist pain Getty Images 1). Oscar Piastri , McLaren
, McLaren 2). Lando Norris , McLaren
, McLaren 3). Max Verstappen , Red Bull
, Red Bull 4). George Russell , Mercedes
, Mercedes 5). Lewis Hamilton , Ferrari
, Ferrari 6). Kimi Antonelli , Mercedes
, Mercedes 7). Charles Leclerc , Ferrari
, Ferrari 8). Pierre Gasly , Alpine
, Alpine 9). Isack Hadjar , Racing Bulls
, Racing Bulls 10). Fernando Alonso , Aston Martin
, Aston Martin 11). Alex Albon , Williams
, Williams 12). Gabriel Bortoleto , Sauber
, Sauber 13). Liam Lawson , Racing Bulls
, Racing Bulls 14). Lance Stroll , Aston Martin,
, Aston Martin, 15). Ollie Bearman , Haas
, Haas 16). Nico Hülkenberg , Sauber
, Sauber 17). Esteban Ocon , Haas
, Haas 18). Carlos Sainz , Williams
, Williams 19). Franco Colapinto , Alpine
, Alpine 20). Yuki Tsunoda, Red Bull Getty Images
Oscar Piastri ended the session half a second clear of teammate Lando Norris, who was on used tires for his best effort, and nearly three-quarters of a second clear of Charles Leclerc in P3 for Ferrari. Max Verstappen was nearly a second off the pace for Red Bull.
Lewis Hamilton endured another frustrating session, ending FP3 down in ninth place, four-tenths of a second back from Leclerc in the sister Ferrari car.
Isack Hadjar is continuing to put in solid displays for Racing Bulls, riding high from his impressive Monaco showing. He ended FP3 sixth, two-tenths clear of Liam Lawson across the garage. Home favorite Fernando Alonso will also take the positives from his run to eighth given Aston Martin's struggle for form this year, leading to his own point-less start to the season. Getty Images
McLaren also topped the standings in FP2, but there was at least a bit of competition at the front with both George Russell's Mercedes and the Red Bull of Max Verstappen within range of Oscar Piastri's fastest lap time on Friday afternoon.
Piastri's best effort saw him dip into the 1m12s range, finishing 0.286 seconds clear of Russell in P2. It came as further encouragement for McLaren, particularly after all the fuss about how the front wing technical directive and clampdown could impact its fortunes. Lando Norris could only muster P4 in the sister McLaren, setting an identical lap time to Verstappen in the Red Bull.
Ferrari appeared to be a little bit of a step behind the leading trio, with Lewis Hamilton falling all the way down to 11th place in that session and reporting on the radio that the car felt 'undriveable.'
To see Lando Norris setting the pace for McLaren on Friday in FP1 was no great surprise.
Norris got a good boost from his Monaco Grand Prix weekend performance, controlling the race from pole position, yet he highlighted the need for consistency moving forward and repeating those kinds of displays. He certainly started on the right foot in Barcelona, finishing three-tenths of a second clear of Max Verstappen at the top of the order.
This was always going to be a track and circuit conditions that should play toward McLaren's strengths, but Norris' early pace also pointed to the impact of the flexi-wing clampdown and technical directive being minimal. Formula 1
In the teams' championship, McLaren now has more than double the points total of its closest rival.
That makes sense with Red Bull, given Max Verstappen has scored 136 of its 143 points. Mercedes are only four more points up the road in second, with Ferrari a solitary point behind the fizzy drinks cars.
Aston Martin is the team that will be looking for some big strides over the coming races. They sit P8, with just 14 points — all of them scored by Lance Stroll. Formula 1
Having seen his McLaren teammate win in Monaco from pole, Oscar Piastri's lead in the drivers' championship over Lando Norris is down to just three points.
Max Verstappen remains in the hunt behind too, especially if his Red Bull benefits from upgrades and updates now Barcelona has arrived.
Meanwhile, Fernando Alonso arrives at his home race without a single championship point this year. The same can be said for Sauber rookie Gabriel Bortoleto and Alpine's Franco Colapinto — although Liam Lawson did finally get on the board with four points and P8 in Monaco. Getty Images
Lando Norris won the 2025 Monaco Grand Prix from pole, ahead of home hero Charles Leclerc and Oscar Piastri in the second McLaren — but the race's story was dominated by a new rule requiring every driver to do two pit stops.
The rule was introduced after the 2024 Monaco race was a lifeless procession following a red flag on Lap 1, and it did produce talking points across the field this year.
Several teams employed tactics that meant one driver helped their teammate by slowing down rivals behind, while fourth-place finisher Max Verstappen stopped for the final time ahead of the final lap, well out of sync with the other leaders.
Our experts, Luke Smith and Madeline Coleman , were in Monaco and you can grab their takeaways from last weekend below.
GO FURTHER
Monaco GP: Lando Norris wins hectic race, Mercedes frustrated by Williams tactics Getty Images
We are rattling through the races in 2025, with our first European races done and dusted.
A trip to Montreal for the Canadian Grand Prix follows this weekend, before the real meat of the European season arrives: 1: Australia — NORRIS (Win & Pole)
— NORRIS (Win & Pole) 2: China — PIASTRI (W&P)
— PIASTRI (W&P) 3: Japan — VERSTAPPEN (W&P)
— VERSTAPPEN (W&P) 4: Bahrain — PIASTRI (W&P)
— PIASTRI (W&P) 5: Saudi Arabia — PIASTRI W (Verstappen P)
— PIASTRI W (Verstappen P) 6: Miami — PIASTRI W (Verstappen P)
— PIASTRI W (Verstappen P) 7: Emilia-Romagna — VERSTAPPEN W (Piastri P)
— VERSTAPPEN W (Piastri P) 8: Monaco — NORRIS (W&P)
— NORRIS (W&P) 9: Spain (Barcelona) — IN PROGRESS
(Barcelona) — 10: Canada (Montreal) — Jun 13-15
(Montreal) — Jun 13-15 11: Austria (Spielberg) — Jun 27-29
(Spielberg) — Jun 27-29 12: Britain (Silverstone) — Jul 4-6
(Silverstone) — Jul 4-6 13: Belgium (Spa) — Jul 25-27
(Spa) — Jul 25-27 14: Hungary (Hungaroring) — Aug 1-3
(Hungaroring) — Aug 1-3 15: Netherlands (Zandvoort) — Aug 29-31
(Zandvoort) — Aug 29-31 16: Italy (Monza) — Sep 5-7
(Monza) — Sep 5-7 17: Azerbaijan (Baku) — Sep 19-21
(Baku) — Sep 19-21 18: Singapore (Marina Bay) — Oct 3-5
(Marina Bay) — Oct 3-5 19: United States (Austin) — Oct 17-19
(Austin) — Oct 17-19 20: Mexico (Mexico City) — Oct 24-26
(Mexico City) — Oct 24-26 21: Brazil (São Paulo) — Nov 7-9
(São Paulo) — Nov 7-9 22: Las Vegas (Nevada) — Nov 20-22
(Nevada) — Nov 20-22 23: Qatar (Lusail) — Nov 28-30
(Lusail) — Nov 28-30 24: Abu Dhabi (Yas Marina) — Dec 5-7
We are already a third of the way through this season. Getty Images
We are here for all your second screen needs and F1 insights, but we love watching sport and we know live pictures have their place too.
So here's where you can watch the track narratives unfold over the course of the Barcelona sessions, alongside our live coverage: U.S.: ESPN
UK: Sky Sports
Canada: TSN
Australia: Fox Sports, Kayo
Global: F1.tv Getty Images
It's lights out in Barcelona at 9 a.m. ET, 6 a.m. PT and 2 p.m. in the UK. The Athletic
Back in the day, Barcelona was the Sakhir of F1 — the venue for winter testing and a track all the teams and drivers knew so well, it could nullify the grand prix weekend.
It was first built as part of the infrastructure for the Barcelona Olympics in 1992 and offers a great mix of high and low speed corners, which on the whole the drivers love. It also tests them physically.
After tight, difficult tracks for racing at Imola and Monaco the two previous weekends, this will feel like blessed relief for the drivers.
Here are the key circuit facts: Circuit length: 4.657 km (2.894 miles)
(2.894 miles) Laps: 66
Lap record: 1:16.330 (Max Verstappen, 2023)
(Max Verstappen, 2023) First GP: 1991 Getty Images
Hello and welcome to our live coverage of today's 2025 Spanish Grand Prix at the Circuit de Barcelona-Catalunya.
Oscar Piastri put in a formidable lap to earn pole position from McLaren team-mate Lando Norris in Barcelona yesterday.
The McLaren drivers will start ahead of reigning world champion Max Verstappen, and the British duo George Russell and Lewis Hamilton.
Stick with us as we begin counting down to today's race. And don't forget that you can get involved by emailing live@theathletic.com.
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The paper I spoke about last week from a primarily Dutch and Minnesota group compared societal recommendations for an ICD vs cardiovascular magnetic resonance imaging (CMR) phenotyping in patients with suspected CS. The key word was 'suspected' CS. In that study, in the European Heart Journal , CMR phenotyping by (1) no late gadolinium enhancement (LGE) and normal EF, (2) no LGE and abnormal EF, (3) pathology-frequent LGE, and (4) pathology-rare LGE, performed better than professional society recommendations for ventricular tachycardia (VT). Dr Kandolin pointed me to an incredible Circulation EP paper from their group in Helsinki on 305 patients with either biopsy-proven CS (just under half) or highly suggestive by criteria. Right away, this is a different population because the first study looked at patients with distant sarcoidosis (say the lungs) and were evaluating for cardiac sarcoidosis while the second study, in Circulation EP this year, studied patients with proven CS. 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Quote: In patients who have no other guideline-based class I or IIa indications, implantation could be considered if LGE mass is >9.9% by the full-width at half-maximum method or the LGE involves >6 LV segments. Less extensive LGE predicted a 5-year SCD/VT rate <7% with an SCD risk of 0.6 per 100 patient-years, and in these patients other EP studies or close surveillance with repeated risk assessments could be discussed at shared decision-making . If you care about CS and risk stratification, this is an excellent paper. It's worthy of a bookmark. I appreciate the feedback because I learned a lot. My one comment — and this is not at all a criticism of the paper (or papers) — but as a doctor I struggle with these risk thresholds. Say in HCM, what if the 5 year-risk is 5% not 6%. Or in this case of CS, the LGE mass is 7% not 9.9%? 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Namely, compared to White catchment areas, communities serving Black and Hispanic have lower rates of OHCA survival. Of course, the causes could be a lot of things, but the research team noted that in Black/Hispanic areas, first responders were less likely to recognize cardiac arrest, police were less likely to respond to a cardiac arrest, and patients were less likely to be defibrillated. Basically, community-level quality of OHCA was less than what it is White catchment areas. And this may explain the differences in survival. I think it explains some of the differences. But OHCA survival rates are complicated, and differences could also be due to severity of disease. My point in highlighting OHCA is that it's one of the highest value interventions in all of medicine. I have spent many hours on this podcast discussing new treatments with marginal benefit. Bystander CPR and an adequate EMS system is hugely valuable. Why? Because only 10% of patients with OHCA in the US survive. Ventricular fibrillation (VF) without CPR or an automated external defibrillator (AED) occurring out of the hospital is nearly 100% deadly. A VF patient depends on the knowledge and availability of his or her neighbors. Since survival is so bad, any tick up is likely highly cost effective. Bystander CPR and public AEDs are nearly free of risk — it's all benefit. I know OHCA care isn't as exciting as the newest ablation catheter, or stent, or new drug, but it's surely a lot higher in value than either of these things. A new tricuspid valve clip or more AEDs in your city? I'd go with the latter every time. So good on the AHA — and the NFL. The other thing I love about promoting OHCA is that it brings communities together for an obviously great and totally uncontroversial cause. Is a Year of Dual Antiplatelet Therapy Magical Thinking? I hesitate to delve into this topic because it is perhaps the most confusing in all of cardiology. But I will, because yet another study finds that 'less is more.' This seems too simple to state, but the idea is that having a metal cage propping open a coronary lesion is neither a fix nor is it free. Metal in the coronary attracts platelets and then clots can form. Stent thrombosis is a medicalized jargon, but it's a terrible outcome because you go from 0% blockage to 100% blockage. The good news is that the body eventually (and usually) forms a layer around the stent protecting it from the circulating platelets. This we call, and, jargon-wise it is a whopper, endothelialization. The problem of course is that antiplatelet drugs are also not free — blocking platelets increases the risk of major bleeding in the gut, kidneys, and brain. So, the quest — and it is a quest — is to find the Goldilocks recipe for preventing thrombotic or clotting events (such as myocardial infarction) with the lowest rate of bleeding. The usual regimen is to use two antiplatelet drugs (aspirin and either clopidogrel or ticagrelor or prasugrel) for a period before switching to single antiplatelet. Perhaps you can see the complexity already. There are four antiplatelet drugs of varying intensity; and there are near-infinite ways to break up time after the stent, and different types of patients. There's acute coronary syndrome (ACS) vs stable coronary artery disease (CAD) patients; there's high-bleeding risk and not-high-bleeding risk patients; and then there are different stents. You start multiplying and you get about a quadrillion different ways to do antiplatelet drugs. Today I will tell you about one recent trial — but know that there are many. The South Korean trial was called 4D-ACS. It was a comparison of two prasugrel-based strategies in about 650 patients who had PCI and stent during an ACS: one group gets one-month of dual antiplatelet therapy (DAPT) (aspirin 100 mg + prasugrel 10 mg, except the prasugrel dose is adjusted to 5 mg for age>75 or body weight < 60 kg vs the control arm: 12 month of DAPT with aspiring 100 mg and prasugrel 5 mg. The primary endpoint is called NACE. Not MACE , but NACE — or net adverse clinical events: death, myocardial infarction (MI), stroke, ischemia-driven revascularization and bleeding. Bleeding also has 5 different grades. This trial measured types 2-5, so minor bleeding was not included. The results: NACE occurred in 4.9% of the 1-month DAPT group and 8.8% of the 12-month DAPT group. The trial was a non-inferiority comparison. This is a good use of non-inferiority. Why? Because the short duration is very much less intense than the standard 12-month DAPT regimen. If it was just as good, it would be a win. Indeed the 4.9% vs 8.8% easily made non-inferiority and in fact with a hazard ratio [HR] of 0.51; 95% CI: 0.27-0.95; P = .034), it also made superiority. The driver of the lower NACE was a 77% lower rate of bleeding in the short duration DAPT arm: 1.2% vs 5.5%. There were almost no differences in thrombotic events such as MI, stroke, ischemia-driven revascularization. I cover this study because it is such a clear result. If using prasugrel, a one-month DAPT regimen is surely better than 12-month DAPT. You would think it's clear now, but it is surely not. First of all, all patients were Korean, and Asians may respond differently to antiplatelets. Second, the study used a type of stent that is not used in the US. Third, what about 1-month DAPT vs 3 months? What about combos of different antiplatelets. Like aspirin/clopidogrel vs clopidogrel. In general, the trend of late is for shorter courses of DAPT. But my solution in real life is to use one of the most important tools in all of medicine: phone-a-friend. I call my interventional cardiology colleague and ask what they think. They've done the stent and a bifurcation stent in the proximal LAD is going to be different from a mid-circumflex lesion. Perhaps I can make these general statements: ACS patients generally require longer DAPT duration (12 months) due to higher thrombotic risk Non-ACS patients most likely can safely use shorter DAPT durations (6 months for DES. Patients with high bleeding risk may benefit from abbreviated DAPT (1-3 months) regardless of presentation P2Y12 monotherapy after initial DAPT period shows promise for reducing bleeding while maintaining efficacy An individual risk assessment may prove helpful in guiding duration and intensity of DAPT. Final comment: if you are having an ST-elevation myocardial infarction (STEMI), you want a stent done fast. If you have chronic CAD, medical therapy first avoids the entire issue of deciding on the combination of antiplatelets. Sadly, this doesn't happen often enough in many places in the US. JAMA Cardiology has published an interesting study looking at the value (or lack of value) in adding Lp(a) into the new PREVENT equation. The first thing to say is that I covered the AHA's PREVENT equation in August of last year. Proponents of PREVENT say it's better than the standard PCE — which outputs 10-year risk of atherosclerotic events. Of course, the proponents of PREVENT don't just say it's better. PREVENT has been validated in observational datasets. PREVENT differs from the pooled cohort equation because it incorporates kidney function, statin use, social determinants of health and removes the race category. It also starts at a younger age. The most provocative aspect of PREVENT is that it simultaneously is felt to be more accurate, but it lowers estimates of CV risk and lowers the number of statin-eligible people. Gulp. Double gulp. Anyways, the question of the JAMA Cardiology study was whether the PREVENT equation can be made better by adding Lp(a) — which as you probably know is mostly genetically determined and, when elevated, is strongly associated with higher risk of CV events. Since race is removed from PREVENT and race can bear on Lp(a), adding it could be very important. Here is that they did. Two databases — UK biobank and MESA. This was big, big data. Both databases have long-term follow-up. Individuals in the database were put into 4 categories: low risk (5%), borderline (5%-7.5%), intermediate (7.5%-20%), and high risk (> 20%) Then they measured 10-year event rates and correlated it with Lp(a) levels overall and by risk category. Of course they do adjustments for age and sex. The main endpoint is the net reclassification improvement or NRI, which is complicated. Let me try to explain: NRI measures how well a new risk prediction model reclassifies people compared to an old model, but it does this by tracking movements in both directions and netting them out. The NRI splits reclassification into events (people who actually had the outcome) and non-events (people who didn't). For each group, it calculates: Proportion who moved up in risk categories minus the proportion who moved down This gives you a net movement figure for each group. The problem comes in relative vs absolute differences. You see this in the NRI studies of coronary artery calcium (CAC) where, when you consider absolute numbers, more people don't have events and are actually misclassified using NRI. I asked the AI tool Claude about this — because Claude helps — and Claude calls this 'The Conceptual Trap,' and I think it's worth talking about. Claude says that people often interpret NRI as "20% improvement in classification" when it's really "20% net improvement after accounting for movements in both directions." The absolute amount of reclassification — which tells you how much the models actually disagree — gets hidden in this netting process. In this study, they measured NRI both categorically — that is, how many moved into a different risk category based on Lp(a) (ie, going from borderline risk to intermediate risk) — and they also measured the NRI category-free (which is simply whether the patient moved up or down in risk at all). They differed — a lot. The category-free NRI for atherosclerotic events using Lp(a) was about .06 (or 6%). Now, the categorical NRI was 10 times lower — at 0.6% The way I would try to translate that is to say that adding Lp(a) reclassifies about 6% of people on a net basis for CV risk, but it is far less valuable for moving people between low, borderline, intermediate and high-risk categories. Here it was less than 1%. Now, the study did something else that is perhaps somewhat useful. They looked at subgroups of people who may get more reclassification. They found that adding Lp(a) resulted in slightly more reclassification for borderline risk and low risk people. But I have to say the differences are quite modest. For instance, the NRI for low-risk CHD prediction was 10% vs 7.5% for intermediate risk. 10% vs 7.5% — it doesn't seem like a big difference. This is a nice effort. Adding Lp(a) helps a little with prediction. A low-risk person who has an Lp(a) may want to take statins. A borderline person with a low Lp(a) may pass. But here's the thing, and I feel it's the same with CAC. I've seen patients for nearly 30 years in middle America, and the vast majority, perhaps 90% of people cannot conceptualize the difference between 7% and 9% vs 13% risk of 10-year events. I've had lipids done recently and I am borderline risk. And I can't really conceptualize 10-year risk of a nonfatal event. Maybe you can. Two reasons I struggle. One is that philosophically, I think much of disease and health is good and bad luck. As in…stuff happens. The second reason I struggle with 10-year risk prediction is relative to Ukraine attacking Russia's planes and the threat of World War III: how much worry should I place in whether my nonfatal CV risk is 7% without Lp(a) vs 9% with Lp(a)? I come back to my bottom-line when it comes to prevention: there are maximizers who want to do everything. For them, Lp(a) seems useless because they are already on aggressive lipid lowering. There are minimizers who aren't taking pills regardless. And for these patients, Lp(a) is also useless. So, for the few who sweat the details, fine — add Lp(a) to the mix. Publishing in EuroPace , a group of prominent researchers re-analyzed the TOPCAT Americas trial looking at the role of AF in predicting bad outcomes in patients with heart failure with preserved ejection fraction (HFpEF). Recall that TOPCAT is one of the most important trials in cardiology. Sadly, it was marred by data irregularities from Russia and Georgia. TOPCAT was spironolactone vs placebo in HFpEF. The hazard ratio (HR) was 0.89 for the composite primary of death, cardiac arrest, or heart failure hospitalization (HHF). The 11% reduction did not reach statistical significance. But all-cause death was 22% in the Americas and only 8% in Russia/Georgia, and the drug had little effect in that region. Further metabolic studies found that a third of patients supposedly randomized to spironolactone had undetectable metabolites. Excluding Russia and Georgia, TOPCAT was positive with a HR of 0.82 and a confidence interval of 0.69-0.98. I think this is a really important point. Ok, now to the EuroPace paper. The problem with studying HFpEF is it is diverse condition — unlike HFrEF. The authors, mostly EP docs, were interested in AF effects in HFpEF. Specifically, whether AF is simply a marker for advanced CV disease or is it an independent risk factor. They made two groups: Study patients who had AF before or at study entry. This was the 'any AF' group. Study patients with ongoing AF who had it at entry. Then they propensity-matched patients with no AF and looked at outcomes. I know, it's pretty easy to predict what will happen. Before I tell you the results, I hope you are thinking: small, hyperdynamic, noncompliant left ventricles are not going to do well with losing the atrial kick when AF occurs. The primary outcome of these comparisons was CV mortality. About 580 patients in TOPCAT who had any AF and 400 had ongoing AF. And they found that: Any AF was associated with a statistically significant increase in CV hospitalization, HHF, and progression of HF. Any AF, however, was not associated with an increased risk of sudden death. Ongoing AF was associated significantly with CVD, pump failure death, CV hospitalizations, and HHF. It was interesting to me that neither any AF or ongoing AF was not strongly associated with sudden death. AF seemed to associate mostly with progression of HF or pump failure. This paper has a lot of complicated comparisons, but I think it can be summarized as AF is a bad thing to have with underlying HFpEF. The question of course, the clinical question, is how to modify this problem with therapy. My first recommendation is to phone-a-friend: your EP colleague. I can't give you a generic right answer because there isn't one. HFpEF patients often have serious comorbidities that have to be considered, things like polypharmacy and CKD and valvular HD and frailty. Maybe antiarrhythmic drugs are the right answer. Maybe ablation. And underused in some places is the 'pace and ablate' strategy. We see a lot more HFpEF these days, because people live longer and with more chronic illness. When AF occurs, it's serious. Take Mr. Rogers' advice and realize that we all need helpers in our lives, and please: call your EP friends.
