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

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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Inflammation: a missing target in coronary heart disease treatment

The role of inflammation in coronary artery disease’s pathophysiology dates back to more than 100 years ago. By the end of the 18th century, Virchow described atherosclerosis as “endarteritis deformans” for the first time. Since then, many studies at the cellular level have shown that lipid accumulation in blood vessels cannot justify the development and progression of the atherosclerosis process. Today, it is established that metabolic factors in conjunction with the inflammatory process lead to the initiation and progression of atherosclerosis. Still, the interaction of innate and adaptive immune systems for the development of atherosclerosis is not fully understood.

Despite significant progress in cardiovascular disease therapies, patients with cardiovascular disease are at high risk of adverse clinical outcomes. Current treatments have focused on lowering low-density lipoprotein-cholesterol concentration, inhibiting platelet activation and coagulation cascades, controlling blood pressure and glucose levels. None of these FDA-approved therapies have targeted the inflammatory pathways involved in atherosclerosis.

Clinical studies have emerged in the cardiovascular field to target inflammation in the past five years. Canakinumab, a monoclonal antibody targeting interleukin-1β, was one of the first anti-inflammatory medications shown to lower the risk of adverse cardiovascular events. In 2017, Ridker and colleagues1 showed that canakinumab led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering among patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. Two years later, in 2019, Ridker and colleagues2 published the efficacy of low-dose methotrexate to prevent atherosclerotic events. Unlike the Canakinumab Anti-Inflammatory Thrombosis Outcome Study (CANTOS), methotrexate-an antimetabolite medication indicated for the treatment of autoimmune diseases and a variety of cancers- not only failed to show any efficacy in lowering adverse cardiovascular events among patients with previous myocardial infarction or multivessel coronary disease but also resulted in elevations in liver enzyme levels, reductions in leukocyte counts, hematocrit levels, and a higher incidence of non–basal-cell skin cancers than placebo. The negative result implies the need for explicitly targeting the inflammatory pathways directly involved in atherosclerosis. In 2020, 2 studies evaluated the efficacy of colchicine in reducing atherosclerotic events. Both studies3, 4 showed that patients with chronic coronary artery disease who received colchicine 0.5mg daily had a lower risk of cardiovascular events compared who received placebo. Lastly, a double-blind, randomized, placebo-controlled phase 2 trial5 evaluated the efficacy of ziltivekimab-a human monoclonal IL-6 inhibitor- among chronic kidney disease patients with elevated high-sensitivity CRP. The study showed that ziltivekimab significantly reduced biomarkers of inflammation relevant to atherosclerosis. The study paves the way for conducting a large-scale cardiovascular outcomes trial to investigate the effect of ziltivekimab at high risk of cardiovascular events.

In today’s practice, monoclonal antibodies targeting interleukins are standard therapies in many medicine subspeciality like oncology (many cancers: lymphoma, leukemia), rheumatology (autoimmune disease: rheumatoid arthritis, gout), gastroenterology (Crohn’s disease), and infectious disease (COVID-19 treatment). In the cardiovascular field, although randomized trials are emerging about the efficacy of monoclonal antibodies targeting inflammatory pathways to reduce the cardiovascular risk in patients with atherosclerotic disease, still further evidence is needed. The role of inflammation in atherosclerosis is well-established, and cardiologists may need to better familiarize themselves with inflammatory pathways involved in atherosclerosis since many anti-inflammatory medications will probably be routinely prescribed in the near future to lower the elevated cardiovascular risk.

References:

  1. Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, Fonseca F, Nicolau J, Koenig W, Anker SD, Kastelein JJP, Cornel JH, Pais P, Pella D, Genest J, Cifkova R, Lorenzatti A, Forster T, Kobalava Z, Vida-Simiti L, Flather M, Shimokawa H, Ogawa H, Dellborg M, Rossi PRF, Troquay RPT, Libby P, Glynn RJ and Group CT. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med. 2017;377:1119-1131.
  2. Ridker PM, Everett BM, Pradhan A, MacFadyen JG, Solomon DH, Zaharris E, Mam V, Hasan A, Rosenberg Y, Iturriaga E, Gupta M, Tsigoulis M, Verma S, Clearfield M, Libby P, Goldhaber SZ, Seagle R, Ofori C, Saklayen M, Butman S, Singh N, Le May M, Bertrand O, Johnston J, Paynter NP, Glynn RJ and Investigators C. Low-Dose Methotrexate for the Prevention of Atherosclerotic Events. N Engl J Med. 2019;380:752-762.
  3. Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, Pinto FJ, Ibrahim R, Gamra H, Kiwan GS, Berry C, Lopez-Sendon J, Ostadal P, Koenig W, Angoulvant D, Gregoire JC, Lavoie MA, Dube MP, Rhainds D, Provencher M, Blondeau L, Orfanos A, L’Allier PL, Guertin MC and Roubille F. Efficacy and Safety of Low-Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381:2497-2505.
  4. Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, The SHK, Xu XF, Ireland MA, Lenderink T, Latchem D, Hoogslag P, Jerzewski A, Nierop P, Whelan A, Hendriks R, Swart H, Schaap J, Kuijper AFM, van Hessen MWJ, Saklani P, Tan I, Thompson AG, Morton A, Judkins C, Bax WA, Dirksen M, Alings M, Hankey GJ, Budgeon CA, Tijssen JGP, Cornel JH, Thompson PL and LoDoCo2 Trial I. Colchicine in Patients with Chronic Coronary Disease. N Engl J Med. 2020;383:1838-1847.
  5. Ridker PM, Devalaraja M, Baeres FMM, Engelmann MDM, Hovingh GK, Ivkovic M, Lo L, Kling D, Pergola P, Raj D, Libby P, Davidson M and Investigators R. IL-6 inhibition with ziltivekimab in patients at high atherosclerotic risk (RESCUE): a double-blind, randomized, placebo-controlled, phase 2 trial. Lancet. 2021;397:2060-2069.

 

“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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Elevated Lipoprotein A, are we ready to intervene?

Lipid abnormalities can be classified into four clinical groups:1) elevated triglycerides, 2) low high-density lipoprotein cholesterol (HDL-C),3) elevated low-density lipoprotein cholesterol (LDL-C), and 4) elevated lipoprotein A.  Lipoprotein A disorder has been the least lipid abnormality studied from a clinical standpoint. Although many mendelian and genome-wide association studies have shown an association between elevated lipoprotein A and risk of incident atherosclerotic cardiovascular disease (ASCVD), the causality relationship still lacks the final corroboration of a randomized Lp(a) lowering intervention clinical trial1.

In 1963, for the first time, Kare Berg described the existence of Lp(a). Lp(a) consisted of apolipoprotein (a) bound to apolipoprotein B-100, an apolipoprotein also found on LDL-C particles. Distinct from other lipoproteins greatly affected by diet and genetics, Lp (a) is determined by more than 90% by individuals’ genetics. Lp(a) is synthesized in hepatocytes and is released into blood circulation. Plasma concentrations of Lp(a) are inversely associated with the size of apolipoprotein(a). It is postulated that small isoforms can be synthesized faster than large ones, and apolipoprotein(a) size can account for up to 70% influence on Lp(a) blood concentration. Other known factors include single nucleotide polymorphisms, sex hormones, inflammatory mediators, and dietary factors2.

Many medications have been tested to lower Lp(a) concentration. A large-scale meta-analysis of 5,256 patients (1,371 on placebo and 3,885 on statin) enrolled in a randomized clinical trial showed that most statins significantly increase Lp(a) concentration by 8-24%3. Niacin may lower Lp(a) concentration by 20-30%. However, studies did not show any significant reduction in risk of ASCVD event, once niacin was added to the medication list of patients already receiving a statin. Estrogen can also lower Lp(a) concentration by 20%; however, the usage is limited due to concern about increasing the risk of thrombotic events. Proprotein convertase subtilisin Kexin type 9 inhibitors (PCSK9 inhibitors) have been shown to lower Lp(a) concentrations. In 2 major PCSK-9 inhibitors clinical trials- FOURIER and ODYSSEY OUTCOME- the fourth quartile of Lp(a) in the treatment arm was associated with a 25% increase risk of major adverse cardiovascular events. This implies the presence of residual risk of ASCVD despite very low LDL-C4. In a recent sub-analysis of ODYSSEY OUTCOME trial, alirocumab reduced Lp(a) concentration. Each 5mg/dl decrease in Lp(a) by alirocumab resulted in a 2.5% reduction in risk of cardiovascular events5. It should be noted that none of the above medications have primarily been initially designed to test the hypotheses of the beneficial effect of medication on Lp(a) concentration.

Genetic studies have shed light on the role of each allele on Lp(a) concentrations and have provided a base for pharmacological intervention. Antisense oligonucleotides (ASO) have revolutionized the treatment of Lp(a). ASOs are short DNA fragments designed complementary for a target messenger RNA. LPA gene transcribes the two alleles of apolipoprotein(a) mRNA. ASO like Pelacarsen binds to the mRNA and generates the mRNA-ASO complex. Hepatocytes recognized this complex as foreign objects, and RNase H1 cleaves the sense strand. Four clinical trials have been conducted to assess the efficacy of ASOs to lower Lp(a) concentrations. All the clinical trials have shown promising results, from 40% to up to 90% reduction in Lp(a) depending on the type of ASO, dosage, and frequency of administrations6.

Currently, the pivotal phase 3 of Lp(a)HORIZON7 (ClinicalTrials.gov Identifier: NCT04023552) randomized controlled trial is enrolling up to 8280 individuals, aged >18 years with Lp(a) ≥ 70 mg/dl and with a history of myocardial infarction, ischemic stroke, or symptomatic peripheral artery disease. Participants are double blindly randomized to receive TQJ230 80 mg injected monthly subcutaneously or placebo and will be followed for the primary outcome of MACE (CV death, non-fatal MI, non-fatal stroke, and urgent coronary revascularization). The estimated primary completion date is May 29, 2025. So, we need to be patient and wait to see if the causal relationship between Lp(a) and ASCVD will be established by 2025.

 

References:

  1. Miksenas H, Januzzi JL, Jr. and Natarajan P. Lipoprotein(a) and Cardiovascular Diseases. JAMA. 2021;326:352-353.
  2. Tsimikas S. A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. J Am Coll Cardiol. 2017;69:692-711.
  3. Tsimikas S, Gordts P, Nora C, Yeang C and Witztum JL. Statin therapy increases lipoprotein(a) levels. Eur Heart J. 2020;41:2275-2284.
  4. Ruscica M, Greco MF, Ferri N and Corsini A. Lipoprotein(a) and PCSK9 inhibition: clinical evidence. Eur Heart J Suppl. 2020;22:L53-L56.
  5. Szarek M, Bittner VA, Aylward P, Baccara-Dinet M, Bhatt DL, Diaz R, Fras Z, Goodman SG, Halvorsen S, Harrington RA, Jukema JW, Moriarty PM, Pordy R, Ray KK, Sinnaeve P, Tsimikas S, Vogel R, White HD, Zahger D, Zeiher AM, Steg PG, Schwartz GG and Investigators OO. Lipoprotein(a) lowering by alirocumab reduces the total burden of cardiovascular events independent of low-density lipoprotein cholesterol lowering: ODYSSEY OUTCOMES trial. Eur Heart J. 2020;41:4245-4255.
  6. Tsimikas S, Moriarty PM and Stroes ES. Emerging RNA Therapeutics to Lower Blood Levels of Lp(a): JACC Focus Seminar 2/4. J Am Coll Cardiol. 2021;77:1576-1589.
  7. Assessing the Impact of Lipoprotein (a) Lowering With TQJ230 on Major Cardiovascular Events in Patients With CVD (Lp(a)HORIZON). https://clinicaltrialsgov/ct2/show/NCT04023552. 2019.

“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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2021 Chest Pain Guidelines from AHA21

2021 Guideline for the Evaluation and Diagnosis of Chest Pain was released in October 2021 and discussed in multiple sessions during AHA21. It was a collaboration between cardiologists, interventional cardiologists, cardiac intensivists, epidemiologists, and emergency medicine specialists. The team has focused on a symptom rather than a disease, making this approach unique. In the U.S, chest pain is the main reason for about 6.5 million emergency department encounters and the second reason patients seek medical attention in an emergency room. Only 5.1 % of ED visits with chest pain were found to have an acute coronary syndrome.  It is imperative to distinguish between life-threatening and benign causes. The new guideline has provided recommendations and algorithms for assessing chest pain based on contemporary evidence. This short blog will summarize the top take-home messages.

In the new guideline, authors refrain from using the term “atypical” chest pain. They have argued that this term may be misinterpreted as benign in nature. They have changed the atypical term to non-cardiac, which is more specific in addressing underlying diagnosis. The guideline emphasizes the uniqueness of chest pain in women. It is estimated that cardiac causes of chest pain are underdiagnosed in this population. Since women are more likely to present with accompanying symptoms, health care professionals should consider these symptoms while obtaining a history. An electrocardiogram should be obtained and reviewed for the presence of ST-elevation myocardial infarction within 10 minutes of ED arrival. Furthermore, in patients with intermediate to high clinical suspicion for acute coronary syndrome (ACS), a supplemental electrocardiogram on leads V7 to V9 is needed to rule out posterior MI. Cardiac troponin is a biomarker of choice for detecting myocardial injury. Authors recommend against the measurement of creatine kinase isoenzyme (CK, CK-MB) and myoglobin for diagnosis of acute myocardial injury.

The guideline panelists have revised the term coronary artery disease (CAD). Previously, CAD was defined as the presence of significant obstructive stenosis (i.e., ≥50%). This revision has broadened the term CAD to those with identified non-obstructive atherosclerotic plaques on prior anatomic and functional testing. This approach may prevent those with non-obstructive CAD from getting overlooked and deprived of optimized preventive measures. The guideline also provides recommendations on selecting optimal diagnostic testing for patients with chest pain. A health care professional should first consider the pretest likelihood of CAD before selecting a cardiac test modality. The guideline emphasizes the lack of need to pursue any diagnostic test in those with low CAD risk. A coronary artery calcium score may be appropriate for atherosclerotic cardiovascular disease risk stratification. In patients at intermediate-high risk of CAD, based on age (≥65 years of age vs. < 65 years of age) and suspicion of a degree of coronary obstruction, the guideline recommends further anatomical testing. Coronary computed tomography angiography is favored among patients at a younger age or less obstructive CAD suspicion, while stress testing is preferred among older patients or more obstructive CAD suspicion. The goal of CCTA is to rule out obstructive CAD or to detect non-obstructive CAD. If an evaluation is required, it will also provide further information about the anomalous coronary arteries, aorta, and pulmonary arteries. Ischemia-guided management is the goal of stress imaging. It can provide information when prior CCTA is inconclusive and about myocardial scar tissue and coronary microvascular dysfunction.

The term CHEST PAIN represents the take-home message of the guideline, as shown in the figure. Each alphabet has a meaning. C: Chest pain means more than a pain in the chest, H: High sensitivity troponin is preferred. E: seek Early care for acute symptoms. S: Share the decision-making, T: Testing not routinely needed in low-risk patients. P: use clinical decision Pathways. Accompanying: women may be more likely to present with Accompanying symptoms. I: Identify patients most likely to benefit from further testing. N: Noncardiac is in, and atypical is out. S: Structured risk assessment should be used.

 

“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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The pursuit of Ideal cardiovascular health: It’s never too LATE! But the earlier, the better!

“Cardiovascular health after 10 years: What have we learned and what is the future” was my topic of choice from this year’s AHA21 main scientific sessions. It has been over 10 years since American heart Association (AHA) published a formal definition of cardiovascular health (CVH). In the last 10 years, more than 2,000 publications have tried to address the concept of CVH. AHA 2020 impact goal was to improve the CVH of ALL Americans by 20%, while reducing deaths from cardiovascular (CV) disease and stroke by 20%. Seven key health metrics were used to define CVH including: smoking status, physical activity, healthy diet, blood glucose level, blood cholesterol level, and blood pressure. Each metric was stratified into three statuses: poor, intermediate, and ideal. The initial approach was to improve individuals’ health from poor status into intermediate status and subsequently to ideal status and later promote and preserve ideal CVH through individual’s life(1).

In the last 10 years, many community-based cohort studies including Atherosclerosis Risk in Communities (ARIC), Multi-Ethnic Study of Atherosclerosis (MESA), Women’s Health Initiative (WHI), Coronary Artery Risk Development in Young Adults Study (CARDIA), and Cardiovascular Health Study (CHS) have investigated the association of CVH metric with CV outcomes. A meta-analysis of 13 studies showed that as the number of Ideal CVH metrics decrease the relative risk of all-cause mortality and CV mortality increase in a linear fashion(2). Moreover, studies have expanded the impact of CVH metrics on other chronic disease like cancer, chronic kidney disease, dementia, chronic obstructive pulmonary disease, and hip fracture(3).

Disappointingly, national data have shown that high CVH is uncommon. Only 7% of U.S. adult population meets the criteria for high CVH, 34% for moderate CHV and 59% for Low CVH group(4). It is estimated that 70% of CV events are attributable to low/moderate CVH and up to 2 million CV events can be prevented if all U.S. adults attained high CVH(5). This implies that potential impact of maintaining high CVH is substantial. The question is how early we should intervene to maintain high CVH.

Prevalence of ideal CVH decline significantly with age. In a study of pooled data from 5 community-based cohort, CVH trajectories were defined starting from age 8 to age 55. 5 unique trajectories have been identified. The prevalence was 30.7% for high rapid decline, 10.3% for intermediate rapid decline, 24.3% for high slow decline, 17.4% for intermediate stable and 17.3% for high stable trajectory(6). These trajectories showed that by age 8, already 20% of 8-year-old children do not have ideal CVH. Loss of ideal CVH metrics occurs at different rate across life span, but late adolescence seems to be a critical time where rapid CVH decline occurs. Moreover, analysis of baseline demographic characteristics by CVH trajectory showed that high stable trajectory is most common among white females and high rapid decline trajectory is most common among African American males. Finally, individuals with high stable trajectory were more likely to have ideal diet and physical activity compared to other CVH metrics at baseline (smoking, blood pressure, glucose, lipid level) suggesting that the best approach to maintain ideal CVH is through promoting healthy behavior.

References:

  1. Lloyd-Jones DM, Hong Y, Labarthe D, Mozaffarian D, Appel LJ, Van Horn L, et al. Defining and setting national goals for cardiovascular health promotion and disease reduction: the American Heart Association’s strategic Impact Goal through 2020 and beyond. Circulation. 2010;121(4):586-613.
  2. Guo L, Zhang S. Association between ideal cardiovascular health metrics and risk of cardiovascular events or mortality: A meta-analysis of prospective studies. Clin Cardiol. 2017;40(12):1339-46.
  3. Ogunmoroti O, Allen NB, Cushman M, Michos ED, Rundek T, Rana JS, et al. Association Between Life’s Simple 7 and Noncardiovascular Disease: The Multi-Ethnic Study of Atherosclerosis. J Am Heart Assoc. 2016;5(10).
  4. Virani SS, Alonso A, Aparicio HJ, Benjamin EJ, Bittencourt MS, Callaway CW, et al. Heart Disease and Stroke Statistics-2021 Update: A Report From the American Heart Association. Circulation. 2021;143(8):e254-e743.
  5. Bundy JD, Zhu Z, Ning H, Zhong VW, Paluch AE, Wilkins JT, et al. Estimated Impact of Achieving Optimal Cardiovascular Health Among US Adults on Cardiovascular Disease Events. J Am Heart Assoc. 2021;10(7):e019681.
  6. Allen NB, Krefman AE, Labarthe D, Greenland P, Juonala M, Kahonen M, et al. Cardiovascular Health Trajectories From Childhood Through Middle Age and Their Association With Subclinical Atherosclerosis. JAMA Cardiol. 2020;5(5):557-66.

“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.”