{"id":128924,"date":"2023-01-09T16:31:56","date_gmt":"2023-01-09T16:31:56","guid":{"rendered":"https:\/\/ccs.ca\/?post_type=guideline&p=128924"},"modified":"2023-04-12T04:59:22","modified_gmt":"2023-04-12T04:59:22","slug":"chapter-4-prevention-of-hf-and-asymp","status":"publish","type":"guideline","link":"https:\/\/ccs.ca\/guideline\/2017-heart-failure-management-of-hf\/chapter-4-prevention-of-hf-and-asymp\/","title":{"rendered":"4. Prevention of HF and Asymp"},"content":{"rendered":"\n
HF often progresses from asymptomatic LVSD to symptomatic HF.[16]<\/a><\/sup> Early detection of LVSD might allow intervention on contributing risk factors and pharmacotherapy to delay or reverse the progression of adverse LV remodelling. Data on medications, including ACEs, ARBs, and \u03b2-blockers are summarized online in evidence reviews at www.ccs.ca. Conventional risk factors for cardiovascular disease (CVD) are often included in clinical assessment but a detailed family history might also uncover genetic causes or susceptibility to the development of LV dysfunction. The use of NPs might be useful to identify individuals who are at higher risk for the development of HF and in whom preventative strategies have been studied. The cut point used in the Saint Vincent S<\/strong>creening to<\/strong> P<\/strong>revent H<\/strong>eart F<\/strong>ailure (STOP-HF)[17]<\/a><\/sup> trial of BNP > 50 pg\/mL to undergo echocardiography and collaborative care resulted in a higher rate of use of renin-angiotensin-aldosterone system inhibition therapies, fewer HF events, and significant reduction in hospitalizations for major cardiovascular events over a follow-up on an average of 4.2 years. The NT-proBNP Selected P<\/strong>reventio<\/strong>n of Cardiac Even<\/strong>ts in a Populat<\/strong>ion of Di<\/strong>abetic Patients Without a<\/strong> History of C<\/strong>ardiac Disease (PONTIAC) study[18]<\/a><\/sup> used a cut point of NT-proBNP > 125 pg\/mL to apply further cardiology consultation and individualized \u03b2-blockade and renin-angiotensin-aldosterone system uptitration. Patients in the group randomized to intensified therapy had a 65% relative risk reduction (RRR) in the primary combined event rate of hospitalization or death due to cardiac disease at 2 years. Therapies used in these 2 trials are guideline-based, reinforcing the opportunity to enhance neurohormonal therapy in all individuals with cardiovascular risk factors, limited only by the availability of NP measurement to identify patients. Exercise as a strategy to prevent ischemic heart disease has supported guideline recommended minimum physical activity of at least 150 minutes per week of moderate intensity activity (approximately 500 metabolic equivalents of task minutes). A meta-analysis of 12 prospective cohort studies by Pandey et al.[19]<\/a><\/sup> reported the risk of HF is reduced by 10%, 19%, and 35% in people who were participating in leisure activity of 500, 1000, and 2000 metabolic equivalents of task minutes per week, respectively, compared with individuals with no physical activity. This article noted an inverse dose-response relationship between physical activity and development of HF. The importance of prevention of HF is supported by evidence that preventing and treating cardiovascular risk factors and conditions that cause atherosclerotic disease leads to fewer patients developing HF. Many of these risk factors also contribute to the development of HF independently from atherosclerotic disease (Table 3). Previous HF guidelines have reviewed the substantial evidence supporting the screening and management of common risk factors for the development of HF such as hypertension, diabetes, smoking, dyslipidemia, obesity, alcohol use, and sedentary behaviour.[20]<\/a>–[27]<\/a><\/sup> Patients with established coronary artery disease (CAD) and\/or previous acute coronary syndrome (ACS) should have these appropriately treated to prevent future HF events.<\/p>\n\n\n\n