guidelines

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Key Takeaways From the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure

Andi Shahu, MD, MHS

What’s new in the treatment of heart failure? The 2022 AHA/ACC/HFSA Guideline for the Management was just released in the beginning of April! While much of the ground it covers might not seem particularly groundbreaking to anyone who has been paying attention to discussions on #MedTwitter, #CardioTwitter or the latest clinical trials over the last 2-3 years, it codifies the guideline directed medical therapy (GDMT) that we have all come to know and love for the treatment of heart failure with a reduced ejection fraction (HFrEF). These new guidelines also provide the first-ever guideline recommendations for patients with (heart failure with a preserved ejection fraction) HFpEF and heart failure with mildly reduced ejection fraction (HFmrEF), though the strength of recommendation for these conditions is not as strong as those for HFrEF.

Here are some key takeaways from the new heart failure guideline!

  1. Quadruple therapy GDMT for HFrEF

The latest guideline officially provides class IA recommendations for the use of the following medications in the treatment of HFrEF (defined as LVEF 40% or lower) in patients that have at least NYHA class II symptoms:

  1. Angiotensin-converting enzyme (ACE) inhibitors (ACEi) [i.e. lisinopril] or angiotensin-receptor blockers (ARBs) [i.e. losartan] or angiotensin receptor blocker/neprolysin inhibitor combination (ARNi) [i.e. sacubitril-valsartan]
  2. Beta blockers [i.e. metoprolol, carvedilol]
  3. Mineralocorticoid antagonists [i.e. spironolactone]
  4. SGLT2 inhibitors (SGLTi) [i.e. empagliflozin, dapagliflozin]

The first three classes were previously recommended for the treatment of HFrEF but prior American cardiovascular society guidelines did not include such a strong recommendation for the use of SGLT inhibitors.

  1. We now have HFimpEF

HFimpEF now refers to heart failure in someone who previously had HFrEF but whose LVEF has improved to >40%. The guideline strongly recommends continuing GDMT for patients that fall into this category.

  1. We now have HFmrEF recommendations

The guideline now provides a class 2A recommendation for the use of SGLT2i in the treatment of symptomatic HFmrEF (defined as LVEF 41-49%). It also provides class 2B recommendations for the use of ARNi/ACEi/ARB, beta blockers and MRAs in these patients. These recommendations confirm what some physicians/cardiologists have already begun doing in practice, though the level of evidence to support the use of these medications in HFmrEF as it is for patients with HFrEF.

  1. We also have new HFpEF recommendations

For the first time ever, the guideline recommends medications for the treatment of symptomatic HFpEF (defined as LVEF 50% or greater). Similar to its recommendations for the treatment of HFmrEF, it provides a class IIA recommendation for the use of SGLT2i and class 2B recommendations for beta blockers, ARNi, ACEi, ARB and MRAs, especially if the patient has an LVEF that is closer to 50%. Again, as we know, the level of evidence to support these practices is not as strong as it is for HFrEF. Still, this represents a change from previous guidelines which provided limited options for treatment of HFpEF.

  1. ICD or CRT is still recommended for primary prevention in certain cases

This guideline continues to recommend an implantable cardioverter-defibrillator (ICD)  in a subset of patients, particularly those whose LVEF remains less than or equal to 35% despite being on maximally-tolerated GDMT (there are nuances to this that we will not get into here). Similarly, as before, the guideline also continues to recommend cardiac resynchronization therapy (CRT) for patients who have an LVEF less than or equal to 35%, sinus rhythm, left bundle branch block with a QRS duration of at least 150 ms, NYHA class II-III symptoms.

  1. New recommendations for diagnosis and treatment of cardiac amyloidosis

The new guideline provides class I recommendations for checking serum and urine immunofixation electrophoresis and serum free light chains in patients (which would help diagnose AL amyloidosis) in patients for whom there is clinical suspicion for cardiac amyloidosis. Similarly, there is a class I recommendation for bone scintigraphy to evaluate for transthyretin (TTR) amyloidosis in patients for whom there is sufficient clinical suspicion for amyloidosis (left to the clinician’s judgment). Genetic testing is also recommended if a patient is diagnosed with TTR amyloidosis. For the first time, the guideline provides a class IB recommendation for the use of tafamadis in patients with transthyretin cardiac amyloidosis. And finally, the guideline gives a class IIA recommendation for use of anticoagulation in patients with concurrent atrial fibrillation and cardiac amyloidosis, regardless of CHA2DS2-VASc score.

 

“The views, opinions, and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness, and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions, or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your health matters. If you think you are having a heart attack, stroke, or another emergency, please call 911 immediately.”
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2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure

Reza Mohebi, MD

The 2022 American College of Cardiology (ACC) meeting was held in Washington DC. It was the first ACC meeting offering both in-person and virtual participation. After two years of uncertainty about the future of scientific meetings, hopefully, the COVID-19 pandemic was under control, and the cardiovascular community had the opportunity to meet colleagues, friends, and mentors/mentees once again. A day before the conference, the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure was released. A year ago, the 2021 Expert Decision Pathway for heart failure Treatment Optimization was released; however, the emerging new therapies available for heart failure necessitate the early update of heart failure (HF) guideline.

Guideline directed medical therapy (GDMT) for heart failure with reduced ejection fraction (HFrEF: LVEF EF≤ 40%) and heart failure with mildly reduced ejection fraction (HFmrEF: LVEF 41%–49%) now includes four-pillar medications: sodium-glucose cotransporter 2 inhibitor (SGLT-2i), angiotensin receptor neprilysin inhibitor (ARNI)/ angiotensin-converting enzyme inhibitor (ACEi)/angiotensin receptor blocker (ARB), beta-blockers and mineralocorticoid receptor antagonist (MRA). New recommendations for patients with heart failure with preserved ejection fraction (HFpEF: LVEF ≥ 50%) were made for the first time. SGLT2i (Class of Recommendation 2a), MRAs (Class of Recommendation 2b), ARNIs (Class of Recommendation 2b), and ARB (Class of Recommendation 2b) are now the cornerstone of HF therapies in patients with HFpEF. Avoidance of routine use of nitrates or phosphodiesterase-5 inhibitors (Class of Recommendation 3: No Benefit) was endorsed in this patient population. Health care professionals also need to understand drugs that may worsen HF. In patients with HFrEF, non-dihydropyridine calcium channel-blocking, class IC antiarrhythmic medications and dronedarone, thiazolidinediones, dipeptidyl peptidase-4 (DPP-4) inhibitors (Saxagliptin and Alogliptin) and Non-steroidal anti-inflammatory drugs should be avoided (Class of Recommendation 3: Harm). In patients with HFrEF without a specific indication, such as atrial fibrillation, or venous thromboembolism, anticoagulation is not indicated (Class of Recommendation 3: No Benefit).

The new guideline also revised the definition for HF stages. Stage A (At risk for HF) was defined as patients with hypertension, cardiovascular disease, diabetes mellitus, obesity, exposure to cardiotoxic agents, or a family history of cardiomyopathy. Stage B (Pre-HF) was defined as patients without current or previous HF symptoms/signs but evidence of structural heart disease, increased filling pressures or elevated stress cardiac biomarker (persistent elevated cardiac troponin or natriuretic peptide). Stage C: patients with current or previous symptoms/signs of HF, and stage D (advanced HF): patients with marked HF symptoms that interfere with daily activity with recurrent hospitalization despite optimized GDMT. The guideline provides therapies for patients at each stage of HF to prevent the progression of HF.

Moreover, the 2022 HF guideline endorsed five additional therapies once GDMT has been optimized. Ivabradine (Class of Recommendation 2a) was recommended for patients with HFrEF, New York Heart Association (NYHA) I-III, in normal sinus rhythm, heart rate ≥70 beats per minute on a maximally tolerated beta-blocker. Vericiguat (Class of Recommendation 2a) for patients with LVEF <45%. Digoxin (Class of Recommendation 2b) for symptomatic HFrEF. Polyunsaturated fatty acids (Class of Recommendation 2b) for HF NYHA II-IV and potassium binders (Class of Recommendation 2b) for patients with HF with hyperkalemia while taking renin-angiotensin-aldosterone system inhibitors. Further recommendations were provided for select patients with HF and anemia, iron deficiency, hypertension, atrial fibrillation, malignancy, sleep disorder, and mitral regurgitation. I would highly recommend my blog readers to review this enlightening just-released HF guideline: https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063

“The views, opinions, and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness, and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions, or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your health matters. If you think you are having a heart attack, stroke, or another emergency, please call 911 immediately.”

 
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Clinical Practice Guidelines Part 1: Why and How Are They Developed

Ahmad Ozair, MD

Clinical practice guidelines find extensive usage worldwide amongst both researchers and clinicians. In 2021, I had the opportunity to act as one of the trainee members of two guideline groups of the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) with the experience being transformative. The following will be a multi-part series on the why’s and how’s of guidelines, getting behind the scenes on their development.

Need for Clinical Practice Guidelines

The American Heart Association (AHA) and the American Stroke Association (ASA), often in conjunction with the American College of Cardiology, produce major clinical practice guidelines (CPGs) that are both widely utilized as professional practice standards globally and used extensively for research. For instance, the guideline papers on ‘Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults’ by the AHA/ACC Task Force on CPGs, which were published in multiple journals simultaneously, have been cited thousands of times by the end of 2021 since their publication in 2017, while having been utilized by millions of clinicians worldwide [1].

These guidelines are critically valuable tools for practitioners, many of whom lack the time to appraise the primary literature themselves. The latter becomes an especially challenging endeavor given the increasing amount of publications along with the expanding number of low-quality studies. In her book, Trisha Greenhalgh had quoted Stephen Lock, who had described in 1979 as the editor of the British Medical Journal, “Few things are more dispiriting to a medical editor than having to reject a paper based on a good idea but with irremediable flaws in the methods used” [2]. In 1994, Douglas Altman, one of the pioneers of the EBM movement, had written those widely quoted words that “We need less research, better research, and research done for the right reasons” [3]. A decade later, John Ioannidis had published his landmark work ‘Why most published research findings are false’ [4].

Twenty years after Altman’s editorial in BMJ, the editor of BMJ wrote how little had changed since then [5]. Chalmers and Glasziou have classically described the four stages of research waste [6], which coupled with the predicted doubling time of medical knowledge reaching 73 days in 2020 [7], leads to the increasing difficulty of reading and synthesizing the primary evidence for oneself. Thus, in an age of information overload, appropriately developed and concisely written guidelines in one part of the world often become a critically valuable tool globally.

Guidelines also help define the value judgments we assign to the primary evidence. For instance, for acute management of ischemic stroke, different anticoagulating drugs may be drugs, with one negative outcome assessed in the literature being the risk of intracranial hemorrhage. Here one value judgment is the significance we assign to the occurrence of intracranial hemorrhage. Finally, for outcomes where high-quality primary evidence is lacking, guidelines may still provide conditional recommendations with low certainty, which are useful to the frontline healthcare worker.

Evolution of Clinical Guidelines

Guideline development has come a long way from before the advent of the evidence-based medicine (EBM) movement to after the widespread utilization of the same. Colloquially, the old approach to guideline development was the GOBSAT model, i.e. ‘Good Old Boys Sitting Around A Table’ [8,9]. This typically was based on a panel of experts (typically males) who would be invited by a professional society to convene for a few days. They would provide their opinion and discuss their clinical practice, and their consensus would get written up as the professional society guideline to be followed worldwide. Many times, this gathering would occur in a hotel or trip funded by a pharmaceutical corporation [9].

In addition, this approach majorly ignored conflicts of interest amongst the experts themselves, since no rules existed on who could participate as a panel member based on their competing interests. Experts, who were paid speaking fees or honoraria related to certain medications by pharmaceutical corporations, would overwhelmingly represent members of the task force making the guidelines on diseases where those drugs would get utilized [9]. These competing interests meant that guideline development had significant bias from the start.

Finally, even if subject matter experts did not have competing interests, it was still likely that their perspective of the literature in totality on the PICO was biased, as was well captured in seminal papers by Mulrow in BMJ and Antman et al in JAMA [10,11]. These authors demonstrated that traditional narrative review-based consensus opinions of experts greatly lagged behind and sometimes significantly differed from effect estimates from well-performed meta-analyses.  In one of their classic examples, Antman et al used the process of cumulative meta-analysis to show that data was consistently building up regarding the futility of lidocaine in improving survival in acute myocardial infarction for many years, yet most major traditional reviews continued to wholeheartedly recommend this medication even after 1990 [11].

Current Model of Guideline Development: An Overview

One of the most widely cited definitions for CPGs or ‘guidelines’ was given by an influential Institute of Medicine (IOM) report which referred to them as “statements that include recommendations, intended to optimize patient care, that are informed by a systematic review of evidence and an assessment of the benefits and harms of alternative care options” [12]. This definition can be broken down into two parts: (A) a systematic review of the primary evidence, which is the groundwork of the guideline, and (B) a set of recommendations, which incorporates both the evidence and the value judgments. The systematic review is typically informed by one of more key questions, that are structured in the PICO format, i.e. Population, Intervention, Comparator, Outcome(s).

Guidelines today are developed by a multidisciplinary panel of experts, which include but are not limited to, subject matter experts (which were the only members of guidelines previously), guideline methodologists, health economists, statisticians, librarians, patient representatives, amongst others (Figure 1). The goal now is to have guidelines that focus on what matters to the patients, and therefore, the outcomes used for decision-making in the guidelines have shifted gradually towards patient-reported outcomes (PROs). Instead of conventional outcomes like blood loss, PROs include pain score, quality of life, time to return to activities of daily living, etc.

Figure 1: Overview of the guideline development process, as seen from the Guideline International Network (GIN)-McMaster Checklist. Reproduced from Piggott T, Langendam M, Parmelli E, et al. Bringing two worlds closer together: a critical analysis of an integrated approach to guideline development and quality assurance schemes. BMC Health Serv Res. 2021;21(1):172. Published 2021 Feb 24. doi: https://doi.org/10.1186/s12913-020-05819-w  under CC BY-NC-SA 4.0 license (https://creativecommons.org/licenses/by-nc-sa/4.0/).

Guidelines, including those of the AHA/ACC now explicitly attempt to reduce distortions, biases, and competing interests. They aim to minimize this by following a pre-specified, explicit, and transparent set of rules, that apply to all guidelines published by that organization. These guidelines have their foundation as the best available systematic review of the primary evidence. The goal is to use this systematic review and provide recommendations with ratings of the quality of evidence (high, low) along with the strength of recommendation (strong, conditional) [13]. Guidelines in the current age are expected to provide clear descriptions of the relationships between health outcomes and different care options.

Finally, guidelines today are revised regularly as deemed appropriate (by a designated group of individuals) to ensure new evidence gets incorporated in a timely manner [13]. For instance, the 2017 ACC/AHA Guidelines on hypertension [1], received an update through an AHA Scientific Statement published in 2021 on the management of stage 1 hypertension in patients with low ASCVD risk.

In the next part of this series on guidelines, we will continue with what principles guide guideline development.

 

“The views, opinions, and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness, and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions, or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your health matters. If you think you are having a heart attack, stroke, or another emergency, please call 911 immediately.”
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DAPA-CKD: Is SGLT2i the ANSWER? Will the guidelines change?

Noora Alhajri, MD, MPH

Over the past years, series of clinical trials prove the beneficial effect of glucose cotransporter 2 (SGLT2) inhibitors in reducing the risk of cardiovascular events in people with type 2 diabetes mellitus. The results from these trials were consistent, significant, and demonstrated a considerable reduction in heart failure hospitalization among patients who used SGLT2 inhibitors, whereas the benefit on atherothrombotic events such as myocardial infarction and stroke was moderate.

Similar findings from The Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation trial (CREDENCE) were obtained for patients with type 2 diabetes mellitus and chronic kidney disease who are exceptionally at higher risk for cardiovascular disease. In CREDENCE trial, Canagliflozin reduced the risk of chronic kidney disease, cardiovascular death or hospitalization, myocardial infarction, and stroke. Although diabetes is not the only cause of chronic kidney disease, and people with chronic kidney disease are still at increased risk for cardiovascular disease, regardless if they had a preexisting history of cardiovascular disease or not. Therefore, its essential to implement guidelines that recommend the use of certain therapeutics as routine treatment for primary and secondary prevention of cardiovascular disease in patients with chronic kidney disease, regardless of their diabetes status.

During #AHA20, I enjoyed attending the online session by Dr. John McMurray, where he shared scientific breakthrough results from the Dapagliflozin And Prevention of Adverse Outcomes in Chronic Kidney Disease (DAPA-CKD) Mega-Trial. The session reported the results of the effect of dapagliflozin on prespecified kidney and cardiovascular outcomes in patients with chronic kidney disease with and without diabetes. The DAPA-CKD trial was a randomized, double-blind, placebo-controlled, multicenter trial, where adults with or without type 2 diabetes, with estimated glomerular filtration rate (eGFR) between 25 and 75 ml/min/1.73 m2, and a urinary albumin-to-creatinine ratio (UACR) between 200 and 5000 mg/g were eligible for DAPA-CKD trial. In this trial, patients were randomized to dapagliflozin 10 mg once daily or placebo with follow up at 2 weeks, 2,4, and 8 months and at 4 months intervals thereafter. The primary composite outcome was the time to the first occurrence of any of the following: > 50% decline in eGFR, onset of end-stage renal disease, or death from kidney or cardiovascular disease. Moreover, secondary outcomes were: 1) kidney composite outcome identical to the primary endpoint with the exception of death from cardiovascular death 2)( a cardiovascular composite outcome consisting of hospitalization for heart failure or death from cardiovascular  causes; and 3) death from any cause.

 

Effects of dapagliflozin on prespecified clinical outcomes according to the baseline history of cardiovascular disease.

 The DAPA-CKD trial found that among patients with cardiovascular disease who received dapagliflozin, the primary composite outcome occurred in 11.2% participants, while the primary outcome occurred in 17.2% in participants who were in the placebo group, (HR 0.61; 95% CI, 0.47-0.79) and the corresponding numbers in people without cardiovascular disease were 7.9% and 12.9% respectively, (HR 0.61; 0.48-0.78).

The DAPA-CKD trial also found that for both the primary and secondary prevention patients, the event rates favored dapagliflozin for all components of the primary and secondary outcomes, although reduction in cardiovascular risk was not statistically significant.

DAPA-CKD Figure

Additionally, among patients with cardiovascular disease, cardiovascular death or hospitalization for heart failure occurred in 9.3% of participants in the dapagliflozin group and 12.8% of participants in the placebo group, (HR 0.7; 0.52-0.94) and the corresponding numbers for patients without cardiovascular disease were 1.8% and 2.7% respectively, (HR 0.67; 0.40-1.13). The observed reduction in cardiovascular risk for these two groups was driven by reduction in heart failure hospitalization which occurred in 4.1% of participants in the dapagliflozin group and 7.3% participants in the placebo group with cardiovascular disease and the corresponding numbers for patients without cardiovascular disease were 0.3% and 1.0% (HR, 0.31; 0.10-0.94) respectively. These results show that dapagliflozin reduced the risk of adverse kidney outcomes irrespective of baseline cardiovascular disease status. Moreover, the mortality benefit from dapagliflozin as demonstrated from the DAPA-CKD study supports the findings of the DAPA-HF trial. In summary, dapagliflozin reduced the risk of kidney failure, death from cardiac disease or hospitalization for heart failure, furthermore, it prolonged survival, in people with chronic kidney disease, irrespective of the presence of a concomitant cardiovascular disease.

 

What is next?

The data from DAPA-CKD trial for dapagliflozin effect on patients with cardiovascular disease and chronic kidney disease is clear, but we have so much work to do. Is Dapagliflozin the answer? How would this change the guideline directed medical therapy (GDMT) for the care of patients with an increased heart failure, cardiovascular or chronic kidney disease risk, regardless of their glycemic status?

 

References:

  1. Effect of Dapagliflozin on Clinical Outcomes in Patients with Chronic Kidney Disease, With and Without Cardiovascular Disease. John J.V. McMurray , David C. Wheeler , Bergur V. Stefánsson , Niels Jongs , Douwe Postmus , Ricardo Correa-Rotter , Glenn M. Chertow , Tom Greene , Claes Held , Fan Fan Hou , Johannes F.E. Mann , Peter Rossing , C. David Sjöström , Robert D. Toto , Anna Maria Langkilde , and Hiddo J.L. Heerspink for the DAPA-CKD Trial Committees and Investigators
  2. Presented by Dr. John J. V. McMurray at the American Heart Association Virtual Scientific Sessions, November 13, 2020.
  3. Heerspink HJ, Stefánsson BV, Correa-Rotter R, et al., on behalf of the DAPA-CKD Trial Committees and Investigators. Dapagliflozin in Patients With Chronic Kidney Disease.N Engl J Med 2020;383:1436-46.
  4. Presented by Dr. Hiddo J.L. Heerspink at the European Society of Cardiology Virtual Congress, August 30, 2020.
  5. Rationale and protocol:Heerspink HJ, Stefansson BV, Chertow GM, et al., on behalf of the DAPA-CKD Investigators. Rationale and protocol of the Dapagliflozin And Prevention of Adverse outcomes in Chronic Kidney Disease (DAPA-CKD) randomized controlled trial. Nephrol Dial Transplant 2020;35:274-82.

“The views, opinions and positions expressed within this blog are those of the author(s) alone and do not represent those of the American Heart Association. The accuracy, completeness and validity of any statements made within this article are not guaranteed. We accept no liability for any errors, omissions or representations. The copyright of this content belongs to the author and any liability with regards to infringement of intellectual property rights remains with them. The Early Career Voice blog is not intended to provide medical advice or treatment. Only your healthcare provider can provide that. The American Heart Association recommends that you consult your healthcare provider regarding your personal health matters. If you think you are having a heart attack, stroke or another emergency, please call 911 immediately.”
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Any Physical Activity is Enough

Bailey DeBarmore

When I was a nutrition intern in 2014, I would excitedly tell patients that walking 30 minutes a day, 5 days a week doesn’t have to be a daunting goal. In fact, research showed that accumulating bouts of 10 minutes conferred cardiac benefits.

Under the often cited “150 minutes/week moderate activity or 75 minutes/week vigorous activity” was the implication that if you couldn’t meet that goal, then why bother?

Did the research specifically say that? Nope. And over the years research on the so-called “Weekend Warriors” has flourished. Is it regular physical activity, or the cumulative amount, that reduces risk?

And then in 2016, the catchy phrase “Sitting is the new smoking” highlighted the birth of a newly emphasized term – physical inactivity – and the distinction between physical activity and exercise.

Earlier this month in Chicago, navigating the bustling 2018 AHA Scientific Sessions, the new Physical Activity Guidelines were revealed. Lo and behold, the news is even better – even a little bit of physical activity is worth it.

It’s not all about aerobic activity, either. We know that resistance training improves insulin sensitivity and helps maintain muscle mass as the human body ages. The result? Less frailty. “Healthy aging”. Fewer injuries from falls, and fewer falls overall.

The new Physical Activity Guidelines didn’t leave that goody out. Upper body weight training even once a week is beneficial – for your heart! Just when you thought you had to huff and puff to beef up your heart health.

With the new Hypertension Guidelines released at Scientific Sessions last year in Anaheim, a renewed effort surfaced for clinicians to encourage lifestyle behavior changes. Not enough time with the patient isn’t an excuse. Research showing that physicians who exercise are more likely to prescribe exercise hit headlines, and the simple fact that clinicians can utilize their position of authority to impart importance upon a topic.

“As a health care provider, you know it’s important to help your patients get more physical activity. But it can be challenging to motivate patients in the short time you spend together.” – Move Your Way, Physical Activity Guidelines 2nd Ed., Health Care Provider Fact Sheet

While not everyone feels comfortable taking on a counseling role with patients, there are key phrases and questions you can use to start the conversation. Check out this short Motivational Interviewing primer, which includes example wording to build rapport with your patient, empower them to make change, and establish a collaborative relationship.

  1. Help them set goals. “Are there activities you’d like to be able to do?” We’ve all heard “I want to be able to pick up my grandkids”. Knowing your patients’ motivations means you can work together to set goals that are important to them.
  2. Meet your patient where they are. Find out what they know, what they perceive as important and as barriers, and suggest small changes. Being able to walk a long driveway to get the mail is a better place to start than jumping from the couch to a 5K.
  3. Let them know what to look for. Instead of “aim for moderate intensity activity”, translate it to perceived exertion. A lazy walk is “I’m comfortable and could maintain this pace all day.” Encourage them to reach a Level 3 to 5 – “Comfortable but breathing harder – sweating a little but feel good and can carry on a conversation – just above comfortable, sweating more, and can still talk easily”. Everyone should start slow and build up to longer durations and higher intensities – take a look at the exertion table below to see what exertion level your patient should start in.

 

 

The new guidelines come with Move Your Way tools and resources to get the message out to your friends and family, your patients, and your community. Interactive tools and widgets, fact sheets and poster, and even videos, can help teach all Americans how they can move their way to move more.

Forming new habits is hard, and lifestyle change is no exception. We know the research, and we have the responsibility to translate that data into actionable information for our patients.

I had the opportunity to recap Scientific Sessions over dinner with my parents. What did I share? Just because you can’t run a marathon doesn’t mean you can’t reap the benefits of physical activity. A little bit goes a long way.