News and Views Live from ESC 2015

News and Views Live from ESC 2015

The European Society of Cardiology (ESC) congress was in London, UK from August 29 to September 2, 2015. Our journalists and contributors blogged live from the conference floor, providing top-line results of the major studies and tidbits from the conference sessions. Scroll through to see how the meeting unfolded. For full coverage of the congress, see our ESC conference page.

    The calm before the storm

    Feeling guilty for taking the tube

    Selfie! with Dr Bhautesh Jani during an interview before his press conference in an hour re: blood pressure, depressive symptoms and cardiometabolic disease. Story to come soon...

    There was a nice press "Welcome to the ESC 2015" today. With 26K registrants, it's the largest ESC congress EVER! An added reason for celebration: Female registrants are up from 15% to now 22%!. The spotlight this year is on "Environment and the Heart" with a focus on air pollution. With 188 Abstract sessions and 20 Hot lines, it was necessary this year to add another press conference so we are bound to learn some great news! . Additionally, Nobel prize laureate E. Blackburn will be chairing and presenting a session on Sunday 30th at 11 Regent’s Park ‘the Hub “Ageing and CV disease-The role of cellular senescence". Check in frequently tomorrow and a few times today for more information from the ESC 2015!!!

    Full news story will come from Deb Brauser, meanwhile Midday naps associated with reduced blood pressure and fewer medications
    The study of 386 middle aged patients (200 men and 186 women, ave age 61 years) with arterial hypertension. assesed idday sleep time, office BP, 24 hour ambulatory BP, pulse wave velocity, lifestyle habits, body mass index (BMI) and a complete echocardiographic evaluation including left atrial size. BP measurements were reported as diastolic and systolic BP.

    After adjusting for other factors such as age, gender, BMI, smoking status, salt, alcohol, exercise and coffee, midday sleepers had 5% lower average 24 hour ambulatory systolic BP (6 mmHg) compared with patients who did not sleep at all midday. Their average systolic BP readings were 4% lower when awake (5 mmHg) and 6% lower while they slept at night (7 mmHg) vs non-midday sleepers
    From the UK, Dr. Bhautesh Jani presented data regarding the impact of high as well as low blood pressure in the depressed population. CVA, MI, CHF and death were all increased, but especially so with higher pressures (83% higher risk of at least one CV event at 4 years in those with high blood pressure and a 36% increase in risk in low BP patients). He suggested that resources should be directed at screening more carefully the depressed population of patients for the presence of hypertension.
    Coffee and heart disease: From Friuli in Udine Italy, Dr. Lucio Mos studied for 12 years the relationship between coffee consumption in young hypertensives and the development of pre-diabetes and the need for hypertension therapy. The HARVEST trial data suggested a relationship between heavy coffee consumption in those who possess the CYP1A2 genotype for slow caffeine metabolism as there was an increased risk of developing pre-diabetes. Heavy drinkers also demonstrated a higher risk of need for treatment for hypertension. Perhaps coffee shops could offer free "do-it-yourself" gene testing with every tall latte?
    TV and PE risk: From Osaka University, research fellow Mr. Toru Shirakawa demonstrated that 5 or more hours of TV watching doubled the risk of fatal PE. This is 6x the risk compared with those who watch less than 2.5 hours per day. Perhaps we should replace our couch with an exercise bike AND stop binge- watching Game of Thrones all in one sitting.

    Dr Ohman interviewed Dr Judith Hochman for Life & Times of Leading Cards

    This morning at ESC, I went to a session titled: Athlete Heart: Detecting the fatally-flawed among the fabulously fit.

    It was a case-based presentation – three cases were presented and then there were concluding remarks from a famous professor.

    The first case came from Prof Michael Papadakis (London, UK). He showed an ECG from a 22-year-old rugby player. He noted anterior t-wave changes in V1-V3. The most concerning disease in this differential diagnosis is ARVC.

    Papadakis then launched into a nice presentation on the non-specificity of t-wave inversions in the anterior precordial leads beyond V2 (but not lateral leads.)

    My take-home was that there are many things that turn t-waves over anteriorly. Endurance sport is one. Young athletes, black athletes and female athletes can have anterior t-wave changes without disease.

    Another tip when looking at t-waves anteriorly is to notice the presence of j-pt and ST-elevation. If present these are good things. When not, be suspicious of disease.

    He showed a black athlete’s ECG with striking t-wave inversion anteriorly but also with j-pt elevation and coved/elevated ST segments. This man had no disease.

    In the second presentation, Dr. Sabiha Gati (London, UK, @s_gati) discussed the issue of trabeculations in the LV. Is it pathologic (non-compaction) or physiologic.

    She showed the case of a former professional mountain-biker, now age 41, who had a funny-looking ECG noted during screening. There were QS patterns in V1-V3 and ST elevation in those leads as well. This ECHO showed intense LV trabeculations.

    The young Dr. Gati then proceeded to discuss the difference between LV noncompaction and normal physiology. There is one.

    My take home was that endurance sport can induce trabeculations as a matter of adaptation. Gati told us to be careful applying current criteria for noncompaction to athletes, as the criteria are not specific and lack prospective validation.

    Her patient had amazing numbers on a stress test, no arrhythmia on long-term monitoring, and no symptoms. The consensus of her case was to reassure but follow-up at one-year.

    In the third session, Professor Andre LaGerche (Melbourne, AU) discussed the RV as the potential weak link in the athlete’s heart. The background is important: namely, the RV takes on a disproportionate increase in pressure and volume stress in an athletic heart.

    LaGerche presented a 21-year-old elite rower with t-wave inversions in V1-V3 discovered on a mandated screening ECG. This led to an echo that showed strikingly bright RV trabeculations and a dense moderator band. Indeed, the “shadows” looked ominous. But were they? This is the question—of so much of echocardiography.

    Before I tell you the results, it’s worth keeping in mind that this young rower reported no problems. As far as he was concerned, he was well.

    Now onto the case. LaGerche reported that the patient had no arrhythmia on long-term monitoring; the MRI showed the same trabeculations, but no other issues.

    The lack of other objective findings led him back to the t-wave inversions in lead V1-V3.

    What follows is a cool tip to remember about the anterior precordial leads—one first taught to me by the late Dr. Charles Fisch: they reflect rotation of the heart.

    LaGerche showed MRI data confirming that one aspect of athletic training can be a clockwise rotation of the heart in the chest—which causes V1-V3 to see more of the RV.

    Ah-ha. That makes perfect sense. One other finding he showed was a series of echocardiograms from a professional cycling team in which “funny-looking” RVs were common.

    The case’s conclusion: the asymptomatic rower owned a physiologic variant.

    Professor Antonio Pelliccia (Rome, IT) concluded the session with a 30-minute recap of where we are now with differentiating an athletic heart from a diseased one. He left us with four main points:

    1) The ECG is still useful. The big challenge comes in educating doctors about its utility. More than 90% of athletes with hypertrophic cardiomyopathy will have an abnormal ECG, the professor emphasized.

    2) Echocardiography is the best first step after an abnormal ECG.

    3) Cardiac MRI is the best imaging tool, and it is mandatory in gray-area cases. This was a little in contrast to a comment LaGerche made about MRI often shows the same thing seen on echo.

    4) Gene tests for suspected hypertrophic cardiomyopathy are difficult to use. He reminded the audience of the common lesson taught by Dr. Ackerman of Mayo: phenotype is king.
    The Line up for first hot line session  
    Sunday 11:00-12:30 Hot Line I AMI 
    BACC: Accurate
    and rapid diagnosis of myocardial infarction using a high sensitivity Troponin
    I 1-hour algorithm
    . Dirk Westermann (Hamburg) 

    DOPPLER CIP. Determining Optimal non-invasive
    Parameters for the Prediction of LV Morphological and Functional Remodeling in
    chronic Ischemia Patients  Frank
    Rademakers (Leuven, Be)

    ALBATROSS: Early aldosterone
    blockade in AMI. Gilles Montalescot (Paris)  

    PRomPT: Peri-infarct zone
    pacing to prevent adverse LV remodeling in patients with very large MI. Gregg
    Stone (New York) 

    CIRCUS: Does cyclosporine
    improve clinical outcomes n STEMI. Michel Ovize (Lyon, France) 

    Line up for the 16:30-18:00
    Hot Line II AF/Pacing

    EAST AF: Efficacy of antiarrhythmic drugs shorterm
    use after catheter ablation for AF

    UNDER-ATP: Efficacy of
    adenosine triphosphate guided ablation for AF: unmasking dormant electrical
    reconduction by ATP.  Both presented by Kazuaki Kaitani
    (Nara-Shi, Japan)

    BELIEF: Effect of empiricial LAA isolation on
    long-term procedure outcome in patients with long-standing persistant AF
    undergoing catheter ablation Luigi Di Biase (New York)

    AEGEAN: Assessment of an
    education and guidance program for apixaban adherence in non-valvular AF  Gilles Montalescot


    There's an Obesity Paradox--Or is there?
    (Late Shift, London. Afternoon Shift, US West Coast where I was a couple days ago)
    One session title that jumped out today at the ESC Congress: Obesity is always bad in cardiovascular diseases. That was the oddly controversial name of an intriguing debate, worded a bit vaguely (ie shrewdly) to allow two sides to the issue, both of which seemed convincing to me.
    Prof Dan Gaita (Timisoara, Romania), argued in favor of the statement using a vast cache of epidemiologic evidence that we're all familiar with; no one in the hall seemed to disagree that obesity is a tremendous risk factor for CV disease and death.
    But then Prof Wolfram Doehner (Berlin, Germany) presented much of the fascinating and perplexing data from observational studies and from clinical trials for a so-called obesity paradox: in general, in people with some advanced cardiovascular diseases, survival tends to go up with BMI. Obesity protects. These aren't new findings, and they recur in study after study. Still we have a hard time believing it.
    Doehner's case, which he's written about before, is that the "reverse epidemiology" associated with obesity with respect to CV disease, the seeming paradox, is in people with established disease. We need to distinguish between obesity as a risk factor for seriously bad illness somewhere down the line, he says, vs obesity in people with, say, post-MI heart failure. The distinction, he says, is critical because of the advice heavy people routinely get from physicians, whether they are sick or not: lose weight. There's clear evidence that the extra weight is dangerous in otherwise outwardly well people. But it's quite unclear that it is in people with advanced CV disease, and the evidence should be respected.
    Here's the hazard: If the patient advised to lose weight is successful--and calorie restriction will inevitably be a big part of it--it turns out to be good for primary prevention but likely bad for secondary prevention, the evidence seems to show. Starvation aggravates catabolic processes associated with the disease, Doehner proposes, making it worse; the patient gets sicker. Maybe--he is speculating--if the sick patients lost weight without restricting calories--such as by exercising more, IF possible--it would not make their condition worse and may improve it.
    So, if that interpretation of the evidence bears up, there is no obesity paradox. But it does have two faces in this debate that are relevant to patient care, according to Doehner: Whether it's dangerous or not dangerous (even possibly good) may depend on whether the patient needs primary prevention or secondary prevention.
    There's more on these sessions to come from the heartwire reporters. This is just the start. Please come back soon and check out this blog and the news and other features on our site.
    #ESCCongress press conference sees another crack at trying to reduce reperfusion injury, this time cyclosporine in STEMI patients.
    The CIRCUS study, led by Dr Michel Ovize, randomized more than 900 patients to cyclosporine or placebo prior to PCI to reduce the risk of reperfusion injury. Cyclosporine had no effect on downstream clinical events, including events related to HF. In fact, the phase 3 trial showed no benefit on infarct size as assessed by peak creatine kinase levels.
    Interestingly, the formulation of cyclosporine differed from the formulation used in an earlier phase 2 study conducted by Dr. Michel Ovize and colleagues. However, Dr. Ovize does not believe the formulation was the reason for the negative CIRCUS results. In fact, he said there is data showing that this formulation of cyclosporine did reduce infarct size (although infarct size was not reduced in CIRCUS). In CIRCUS, which included more than 900 patients, the drug, given prior to PCI, failed to reduce clinical events, including HF outcomes and adverse left ventricular remodeling.
    AEGEAN trial on apixaban (Eliquis) adherence/persistence rates:  Presented by Dr. Giles Montalescot from Paris: This trial aimed to examine the impact of an educational program (including smart phone alerts and easy access to clinic personnel who already staff a warfarin clinic)  on compliance rates.  The BAD news:  Additional education did NOT help.  The good news: By most standards an 88% compliance/adherence rate in both groups (compared to many trials where compliance rates are around 50%) suggested they didn't need education. On the other hand, the 12% who failed to adhere or exhibited low persistence are the ones who REALLY  need education. The trick would be to figure out who they are, why they are the way they are and then target them for improvement.

    BELIEF trial: DON'T leave out the LAA when ablating patients who've been in Afib for longer than one year.  In this trial, patients either got standard ablation (PVI plus extra pulmonary sites therapy) OR PVI/extra pulmonary triggers AND LAA ablation. With no difference in complication rates but a longer procedure time, the effort seems quite worth it:  ONLY 28% of standard ablation patients were recurrence- free at one year (abysmal)  vs. 56% for those who got standard ablation PLUS LAA ablation (less dismal).  Take home:  I'm not sure how strongly one needs to advocate for ablation in this group of persistent afib-ers when the success rate is like flipping a coin,  but if you gotta do it,  at least based on this data, one should add those necessary burns in the LAA.
    The LEADLESS II trial of just over 500 patients is the largest trial yet presented on the topic of percutaneously implanted leadless pacer devices indicated for those with VVI needs (permanent AF) with atrio-ventricular (AV) block (which includes AF with a slow ventricular response), ii) normal sinus rhythm with 2nd or 3rd degree AV block with a low level of physical activity or short expected lifespan, sinus brady with infrequent pauses and EP findings to explain infrequent syncope. "22 serious adverse device effects were observed over six months, including cardiac perforation, device dislodgement, and elevated pacing capture thresholds at rates of 1.3 percent, 1.7 percent, and 1.3 percent, respectively- consistent with that of traditional pacemaker implants. The battery life is projected at 15-21 years, all dislodged devices were retriveable and the need for a pocket is eliminated. (think-elderly cachectic nursing home patients with no sub-q fat to support reasonable wound healing). It's exciting data with limited application, surely it will serve as a stepping stone for future dual chamber needs in this day and age of wireless communication? (My own personal query, no information presented on this topic today). We will certainly be hearing more from the Nanostim in future meetings.
    Does air pollution affect the rate of STEMI? Yes, says the The Belgian study from the Belgian STEMI Registry. Both particulate and NO2 air pollution raised the risk respectively of 2.8% and 5.1% for each 10 ug.m-3 rise. The negative effects of air pollution were observed only in men for reasons unclear, either a statistical gliche due to females representing 20% of the cohorts or an intriguing twist. No baseline characteristics could be blamed either such as the presence of hypertension or pre-existing diabetes. I asked if there was any correlation with smoking when it came to the male vs. female incidence and there was none. Though rates of STEMI were increased, STEMI mortality was not affected by pollution levels.
    And the only positive trial from the Hot Line I session was ...
    BACCAccurate and rapid diagnosis of myocardial infarction using a high sensitivity Troponin
    I 1-hour algorithm

    News editor Steve Stiles noted the failures in strategies to prevent remodeling and enlargement post MI with no benefits seen in PROMPT (Peri-infarct zone pacing to prevent adverse LV remodeling in patients with very large MI) and  DOPPLER CIP ( Determining Optimal non-invasive Parameters for the Prediction of LV Morphological and Functional Remodeling in chronic Ischemia Patients ) 
    Is TEE mandatory in patients undergoing AF ablation with uninterrupted NOACs are used?

    I went to this rapid-fire abstract this morning.

    I don’t like TEEs. It’s a big tube; it’s an extra procedure, and it often adds logistic barriers to getting the ablation procedure done in a timely fashion. Yet, I also don’t want to perform ablation in the setting of LAA clot.

    This is, therefore, an important and timely question. More and more patients come for ablation while taking NOACs. They are doing well on the drugs. Switching to warfarin is not easy.

    An abstract presented this morning at ESC 2015 provides useful information and hints at the fact that TEE may not be necessary—even in patients with persistent AF and high CHADS-VASC scores.

    Here’s the short-version: Dr. L Di Biasi (Albert Einstein College of Medicine, NY) presented data on a prospective multicenter registry of 970 patients treated with either rivaroxaban (n=456) or apixaban (n=514) who had AF ablation. The mean age was 69 years, 85% of the cohort had non-paroxysmal AF, and the mean CHADS-VASC score was 3.

    Zero patients had LAA clot noted on intracardiac echo. That’s not a typo. The group used ICE, maneuvered into the RV outflow tract, to view the LAA appendage. Di Biasi said while showing a slide of an ICE image of the LAA: “why do a TEE, when you can get images like this?” LA smoke was noted in 42% of patients – an unsurprising finding given the advanced disease of this cohort.

    No patient had a clinical stroke. One patient had a positive sub-clinical cerebral ischemic lesion noted on a post-procedure MRI. This patient had missed two doses of rivaroxaban before the procedure.

    Ok… So this is not a clinical trial, but it’s a lot of data on a large high-risk subset patients. It’s consistent with cardioversion data with NOACs and many other smaller studies on using NOACs in the peri-procedure period.

    We are now well into the experience with using NOACs in the peri-procedural time frame and it’s nice to see this reassuring data.
    On the matter of the negative Circus trial, which looked at a bolus injection of cyclosporine to prevent re-perfusion injury in patients with anterior myocardial infarction, I'm not surprised.

    It's hard to believe we can improve the already stunning results of early intervention in acute MI. The best way to prevent re-perfusion injury, it seems to me, is to prevent acute occlusion in the first place.
    From the University of Manitoba Winnipeg, Canada-Dr. Shuangbo Liu proved a correlation between cold weather and STEMI. Daily temperature highs of < 0 degrees C. were most predictive of MI rates with a 7% increased risk for each 10 degree C. drop. in temp. The presence of snow had no impact when temperature was factored into the assessment. Since the risk could be predicted up to 48 hours prior to the MI the potential for education to increase public awareness and help gear up medical systems is not negligible.
    If you met the legend
    earlier today at ESC, you may want to revisit this Life & Times episode from
    2011 featuring
    Prof. Keith Fox interviewed by Dr Rob Califf

    Dr Sam Goldhaber interviewed Dr Charles Pollack on NOAC reversal agents

    Dr Westermann recorded highlights from his earlier presentation of the BACC trial on hsTnI for ruling out/in MI at 1 hour

    This is big news, perhaps the most important from ESC2015 thus far.

    The CHADS-VASC score may be able to predict stroke and death in patients with heart failure but NO atrial fibrillation.

    That's right -- no AF.

    Here is a case:

    You are seeing a 75-year-old female with a history of ischemic cardiomyopathy (EF=35%), HTN and diabetes. She is in sinus rhythm but her CHADS-VASC score, that is, if she had AF, would be 6.

    Without a history of AF, you prescribe aspirin. I don’t know about you, but I worry about stroke and systemic thromboembolism in this sort of patient. You almost wish for a “little” AF so that you can prescribe an anticoagulant.

    An intriguing observational study presented at ESC this morning suggests we need to think about anticoagulants as a stroke prevention strategy in heart failure patients, whether or not they have AF.

    Investigators from Denmark and UK mined the massive data bank available from three Danish health registries to better understand stroke risk in patients with heart failure and no AF. After an analysis of more than 35.000 patients over ten years, the research team found:

    1) Pts w heart failure had a high risk of ischemic stroke, thromboembolism, and death whether or not AF was present.
    2) The CHADS-VASC score modestly predicted these hard outcomes
    3) The CHADS-VASC score had an excellent negative predictive value –low risk patients had truly low risk of events.
    4) Pts with HF without AF who had CHADS-VASC greater than or equal to 4 exhibited a graded increase in absolute risk of stroke, thromboembolism and death.
    5) The absolute risk of any thromboembolic event was higher among patients without AF compared with those patients who had AF.

    My colleague Sue Hughes from Medscape Neurology has stellar coverage of this important study.

    I believe these observations will lead to a fertile area of new research. The idea of using anticoagulants, rather than antiplatelet drugs, in HF patients without AF is intriguing because there are millions of patients with heart failure without AF.

    There is a lot of talk about outcomes in heart failure. People question whether things like admissions and readmissions are useful outcome measures. No one questions stroke or thromboembolism. These are important things to prevent.

    The companies that make NOAC drugs have to be looking hard at these data.

    I’m also wondering about what this data says about stroke mechanisms. There is great overlap in the populations of patients with AF and HF. Stroke does not seem to cluster around AF episodes. If we think of stroke as a manifestation of systemic disease (low flow, platelet aggregation, etc) why wouldn’t we expect HF patients to have a higher risk, regardless of the presence of AF?

    I’m thinking a lot about this study. I’ll write more about it later.
    A 6ng/L cutoff of the TnI assay was better than current European standard of hsTnT At 99th percentile. No FDA approved hsTn test yet. Dr Westermann said each test will need to be validated for ideal cutoff
    Some opinions from the twittersphere on the ESC CHADSVASC study 

    From last year,  Dr Sam Goldhaber recorded a clotblog titled CHA2DS2VASC:
    Useful Beyond A-Fib?

    TECOS: Trial for evaluating cardiovascular Outcomes with sitagliptin in patients with type 2 diabetes. Frans Van De Werf Some data presented at ADA and covered here
    Other trials in Hot Line III session
    ARTS-HF Finerenone versus eplerenone in patients with worsening chronic heart failure with type 2 diabetes mellitus and/or chronic kidney disease

    ELIXA: Evaluation of Lixisenatide in ACS by Eldrin Lewis (Boston) Some previous data reported by Lisa Nainggolian here

    SCOT: The Standard care versus Celecoxib Outcome Trial; a randomised, trial comparing the cardiovascular safety of celecoxib versus traditional non-steroidal anti-inflammatory drugs Thomas MacDonald (Dundee, UK)

    OPTIDUAL: 12 vs 48 months of clopidogrel after DES Gerard Helft

    Up for Monday’s Hot Line IV Session Hypertension

    ATTEMPT-CVD: A trial of Telmisartan prevention of cardiovascular diseases: the large biomarkers study w/ 1228 patients by Hisao Ogawa

    PATHWAY 2: Principal results of the Prevention and
    Treatment of Hypertension w/ Algorithm based Therapy: Optional Treatment of
    drug-resistant hypertension Bryan Williams (London)

    PATHWAY 3: Comparison of single and combination
    diuretics in essential hypertension Morris Brown (Cambridge UK)

    PARAMETER: Principal results of the prospective
    comparison of angiotensin receptor neprilysin inhibitor w/ angiotensin receptor
    blocker measuring arterial stiffness in the elderly Bryan Williams

    Morning press conference for SCOT, ELIXA, TECOS, ARTS-HF, and OPTIDUAL now underway.

    Interesting session later on today at #ESCcongress--should drugs and devices have to clear the same hurdles before getting approved?
    Some big, big names in cardiology will discuss the regulations around approving drugs vs devices: Rob Califf (from the FDA!), Steven Nissen, and Marty Leon, among the notables.
    SCOT pragmatic trial no significant difference in safety between celecoxib and non-selective non-steroidal NSAIDS in patients with osteoarthritis and rheumatoid arthritis over 3.2 year follow up.

    Quote of the press conference "I used to be a regulator but I'm alright now" said Presenter Tom MacDonald (Dundee, Scotland)
    There is NO label warning of risk with sitagliptin. That warning is for SAXAGLIPTIN and it is based on data from the SAVOR TIMI 53 study. Dr. Paul Armstrong (University of Alberta) presenting data showing no risk of HF in TECOS, including multiple subgroups. Important subgroup includes the prior HF patients. No signal of risk with sitagliptin, reports Armstrong.
    OPTIDUAL no statistical difference in MACE or major bleeding in patients with DES randomized to extending dual antiplatelet after 1 year or continuing aspirin only.

    Post-hoc analysis trend for reduction in ischemic events with longer dual therapy. Most patients had second gen DES (1/3 first gen). Trial included clopidogrel only (no prasugrel or ticagrelor)
    There is another diabetes drug on the horizon, one that actually lowers CVD events.

    (Reuters) - A new diabetes pill from Eli Lilly and Co and Boehringer Ingelheim cut risk of heart attack, stroke and death in a closely watched study, the first glucose-lowering drug to show such protective results in a large cardiovascular trial, the drugmakers said on Thursday.

    Besides burnishing the image of the year-old drug, Jardiance (empagliflozin), the results could raise the profile of rival new drugs in the same class of sodium-glucose cotransporter-2 (SGLT2) inhibitors, such as Johnson & Johnson's Invokana (canagliflozin) and AstraZeneca Plc's Farxiga (dapagliflozin).

    If, comments Armstrong, the empagliflozin results remain as robust as hinted at in topline results, then the clinical guidelines for the management of patients with DM would likely change. Until then, researchers and clinicians are looking forward to seeing the data presented and undergo the rigorous peer-review publishing process.

    Dr. Paul Armstrong presents the results of the HF subanalysis from TECOS, a sitagliptin DM trial. #ESCcongress

     Next Hot Line press conference underway on hypertension. Studies to be presented: PATHWAY-2 and 3, ATTEMPT-CVD, and PARAMETER (the one I'll be writing about).

    You can't really tell but Dr Bryan Williams is answering a question after his PATHWAY-2 presentation from our very own Mike O'Riordan. Really!

    Dr. Bryan Williams presented data from PATHWAY-2, a study investigating optimal treatment of patients with resistant hypertension. In patients on the big three antihypertensive medications--RAAS blockade with an ACE inhibitor or ARB, CCB, and diuretic--adding spironolactone is unequivocally the best treatment option, says Williams. Among 300+ patients, adding spironolactone saw patients achieve a home-monitored systolic BP of 134.9 mmHg, with 60% of patients getting to target. Office reductions in BP were even more impressive.
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