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A number of societies produce heart failure (HF) management guidelines, comprising official recommendations on the basis of recent research discoveries, but their applicability to specific situations encountered in daily practice might be difficult. In this clinical practice update we aim to provide responses to fundamental questions that face health care providers, like appropriate timing for the introduction and optimization of different classes of medication according to specific patient phenotypes, when second-line therapies and valvular interventions should be considered, and management of difficult clinical scenarios such as cardiorenal syndrome and frailty. A consensus-based methodology was used. Approaches to 5 different phenotypes are presented: (1) The wet HF phenotype is the easiest to manage, decongestion being performed alongside introduction of guideline-directed medical therapy (GDMT); (2) The de novo HF phenotype requires the introduction of the 4 pillars of GDMT, personalizing the order on the basis of the individuals' biological and physiological characteristics; (3) The worsening HF phenotype is a marker of poor prognosis, and therefore should motivate optimization of GDMT, start second-line therapies, and/or reevaluate goals of care/advanced HF therapies; (4) The cardiorenal phenotypes require correct volume assessment, because renal function usually improves with decongestion; and (5) The frail HF phenotype require special attention, careful drug titration, and consideration of cardiac rehabilitation programs. In conclusion, specific common HF phenotypes call for a personalized approach to improve adoption of the HF guidelines into clinical practice., (Copyright © 2023 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Background: Selecting the appropriate antithrombotic regimen for patients with atrial fibrillation (AF) who have undergone percutaneous coronary intervention (PCI) or have had medically managed acute coronary syndrome (ACS) remains complex. This multi-centre observational study evaluated patterns of antithrombotic therapies utilized among Canadian patients with AF post-PCI or ACS., Methods and Results: By retrospective chart audit, 611 non-valvular AF patients [median (interquartile range) age 76 (69-83) years, CHADS 2 score 2 (1-3)] who underwent PCI or had medically managed ACS between August 2018 and December 2020 were identified by 68 cardiologists across eight provinces in Canada. Overall, triple antithrombotic therapy [TAT: combined oral anticoagulation (OAC) and dual antiplatelet therapy (DAPT)] was the most common initial antithrombotic strategy, with use in 53.8 % of patients, followed by dual pathway therapy (32.7 % received OAC and a P2Y12 inhibitor, and 4.1 % received OAC and aspirin) and DAPT (9.3 %). Median duration of TAT was 30 (7, 30) days. Compared to the previous CONNECT AF + PCI-I program, there was an increased use of dual pathway therapy relative to TAT over time (P-value <.0001). DOACs (direct oral anticoagulants) represented 90.3 % of all OACs used overall, with apixaban being the most utilized (50.5 %). Proton pump inhibitors were used in 57.0 % of all patients, and 70.1 % of patients on ASA. Planned antithrombotic therapies at 1 year were: 76.2 % OAC monotherapy, 8.3 % OAC + ASA, 7.9 % OAC + P2Y12 inhibitor, 4.3 % DAPT, 1.3 % ASA alone, and <1 % triple therapy., Conclusion: In accordance with recent Canadian Cardiovascular Society guideline recommendations, we observed an increased use of dual pathway therapy relative to TAT over time in both AF patients post-PCI (elective and emergent) and in those with medically managed ACS. Additionally, DOACs have become the prevailing form of anticoagulation across all antithrombotic regimens. Our findings suggest that Canadian physicians are integrating evidence-based approaches to optimally manage the bleeding and thrombotic risks of AF patients post-PCI and/or ACS., Competing Interests: Declaration of competing interest James K ChowNone Mary K TanNone Bryan J HarResearch grants and/or speaking consulting honoraria from Abbott, Astra Zeneca, Bayer, BMS/Pfizer, CSL Behring, Novartis, Opsens Amelia MC YipNone Mario PaniaguaNone Basem ElbarouniNone Kevin R Bainey,Research grants and/or speaking consulting honoraria from Astra Zeneca, Bayer, BMS. Jean-Michel ParadisNone Akshay BagaiResearch grants and/or speaking consulting honoraria from Servier, Bayer Inc., BMS/Pfizer, Boehringer Ingelheim, Teleflex, Abbott Vascular, Astra Zeneca, JAMP Pharma, HLS Therapeutics. Robert MarandaResearch grants and/or speaking consulting honoraria from Bayer, Bristol Myers Squibb, CHRC, Novartis, Servier. Investments, Abbvie, Amgen, McKesson Warren J CantorNone Mark J EisenbergNone Jean-Pierre DeryResearch grants and/or speaking consulting honoraria from JAMP Pharma, AstraZeneca, Bayer, BMS-Pfizer, Servier Mina MadanNone Tomas CiezaResearch grants and/or speaking consulting honoraria from Bayer, Boehringer-Ingelheim, Pfizer-BMS, Servier, Lilly, Astra Zeneca Alexis MatteauResearch grants and/or speaking consulting honoraria from Bristol Myers Squibb Sherryn RothNone Shahar LaviNone Anthony GlanzResearch grants and/or speaking consulting honoraria from BMS/Pfizer, Novartis, Bayer, Amgen Dongsheng GaoNone Ravi TahilianiResearch grants and/or speaking consulting honoraria from Pfizer-BMS, Novartis, Bayer, Daiichi Sankyo, Robert C WelshResearch grants and/or speaking consulting honoraria from Astra Zeneca, Bayer, BMS/Pfizer Hahn Hoe KimBMS/Pfizer Simon D RobinsonResearch grants and/or speaking consulting honoraria from Bayer and Servier Benoit DaneaultResearch grants and/or speaking consulting honoraria from BMS/Pfizer, Novartis, Edwards Lifesciences, Bayer, Abbott, Sanofi Aun-Yeong ChongResearch grants and/or speaking consulting honoraria from Servier Michel R Le MayNone Vineeta AhoojaResearch grants and/or speaking consulting honoraria from Amgen, Sanofi, Novo Nordisk, Bayer, Boehringer-Ingelheim, BMS/ Pfizer Jean C GregoireResearch grants and/or speaking consulting honoraria from Bayer, Boehringer Ingelheim, BMS/Pfizer alliance and Servier Pierre-Louis NadeauNone Zachary LaksmanNone Brett HeilbronNone Derek YungResearch grants and/or speaking consulting honoraria from Novartis, Amgen, Boehringer Ingleheim, Pfizer, Abbott, Medtronic, Boston Scientific Kunal MinhasNone Ronald BourgeoisResearch grants and/or speaking consulting honoraria from BMS/Pfizer, Canadian Collaborative Research Network (CCRN), HLS, Novartis Christopher OvergaardNone Hamid BonakdarNone Giridhar LogsettyResearch grants and/or speaking consulting honoraria from BMS/Pfizer Robert DeLaRochelliereNone Samer MansourResearch grants and/or speaking consulting honoraria from Astra-Zeneca, Pfizer, BMS, Sanofi, Amgen, HLS, Boehringer Ingelheim, Servier, Bayer, Abbott Vasculaire, Novartis Caroline SpindlerNone Andrew T YanNone Shaun G GoodmanResearch grant support (e.g., steering committee or data and safety monitoring committee) and/or speaker/consulting honoraria (e.g., advisory boards) from: Amgen, Anthos Therapeutics, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, CSL Behring, Daiichi-Sankyo/American Regent, Eli Lilly, Esperion, Ferring Pharmaceuticals, HLS Therapeutics, JAMP Pharma, Merck, Novartis, Novo Nordisk A/C, Pendopharm/Pharmascience, Pfizer, Regeneron, Sanofi, Servier, Tolmar Pharmaceuticals, Valeo Pharma; and salary support/honoraria from the Heart and Stroke Foundation of Ontario/University of Toronto (Polo) Chair, Canadian Heart Research Centre and MD Primer, Canadian VIGOUR Centre, Cleveland Clinic Coordinating Centre for Clinical Research, Duke Clinical Research Institute, New York University Clinical Coordinating Centre, PERFUSE Research Institute, TIMI Study Group (Brigham Health), (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: The 2021 Canadian Cardiovascular Society guidelines recommend proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitor therapy in patients with atherosclerotic cardiovascular disease whose low-density lipoprotein cholesterol (LDL-C) concentration remains ≥ 1.8 mmol/L despite maximally tolerated statin therapy. This retrospective and prospective observational study characterizes Canadian patients treated with evolocumab and describes its effectiveness and safety., Methods: Between August 2017 and July 2019, a total of 131 patients initiated on evolocumab therapy were enrolled at 15 sites in Canada. Data were extracted from medical records every 3 months between 6 months prior to, and for 12 months following evolocumab therapy initiation, until July 6, 2020. Baseline and prospectively collected data are reported as available., Results: A total of 131 patients were enrolled (59.5% male; mean age [standard deviation (SD)] 64.7 ± 10.6 years), most with a diagnosis of atherosclerotic cardiovascular disease and/or familial hypercholesterolemia (93.4%). Mean (± SD) LDL-C concentration at baseline was 3.7 (± 1.7) mmol/L (n = 119), with 58.0% of patients receiving a statin (36.6% high intensity). Mean (± SD) LDL-C concentration after evolocumab treatment was 1.6 (± 1.0) mmol/L (n = 120), representing a 58.7% decrease from baseline (n = 109). This level remained stable over 12 months. An LDL-C concentration < 1.8 mmol/L was achieved by 77.5% of patients. Persistence was 92%, and no serious treatment-emergent adverse events were reported., Conclusions: These findings provide real-world evidence of guideline-recommended initiation of evolocumab therapy, as well as confirmation of its effectiveness and safety in a Canadian population. Evolocumab therapy can address a healthcare gap in the management of dyslipidemia, by increasing the proportion of patients achieving LDL-C goals recommended to lower cardiovascular risk., (© 2022 The Authors.)

Background: Sodium-glucose cotransporter 2 (SGLT2) inhibition reduces cardiovascular events in type 2 diabetes (T2DM) and is associated with a reduction in left ventricular (LV) mass index. However, the impact on right ventricular (RV) remodeling is unknown. Accordingly, the objective of this study was to assess the impact of SGLT2 inhibition on RV parameters and function in T2DM and coronary artery disease (CAD)., Methods: In EMPA-HEART CardioLink-6, 97 patients with T2DM and CAD were randomly assigned to empagliflozin 10 mg (n = 49) once daily or placebo (n = 48). Cardiac magnetic resonance imaging was performed at baseline and after 6 months. RV mass index (RVMi), RV end-diastolic and end-systolic volume index (RVEDVi, RVESVi) and RV ejection fraction (RVEF) were assessed in blinded fashion., Results: At baseline, mean RVMi (± SD) (11.8 ± 2.4 g/m 2 ), RVEF (53.5 ± 4.8%), RVEDVi (64.3 ± 13.2 mL/m 2 ) and RVESVi (29.9 ± 6.9 mL/m 2 ) were within normal limits and were similar between the empagliflozin and placebo groups. Over 6 months, there were no significant differences in RVMi (- 0.11 g/m 2 , [95% CI - 0.81 to 0.60], p = 0.76), RVEF (0.54%, [95% CI - 1.4 to 2.4], p = 0.58), RVEDVi (- 1.2 mL/m 2 , [95% CI - 4.1 to 1.7], p = 0.41) and RVESVi (- 0.81 mL/m 2 , [95% CI - 2.5 to 0.90], p = 0.35) in the empaglifozin group as compared with the placebo group. In both groups, there was no significant correlation between RVMi and LVMi changes from baseline to 6 months., Conclusions: In this post-hoc analysis, SGLT2 inhibition with empagliflozin had no impact on RVMi and RV volumes in patients with T2DM and CAD. The potentially differential effect of empagliflozin on the LV and RV warrants further investigation., Clinical Trial Registration: URL:  https://www.clinicaltrials.gov/ct2/show/NCT02998970?cond=NCT02998970&draw=2&rank=1 . Unique identifier: NCT02998970., (© 2021. The Author(s).)

Background We studied care gap in patients with familial hypercholesterolemia (FH) with respect to lipid-lowering therapy. Methods and Results We enrolled patients with cardiovascular disease (CVD) or FH and low-density lipoprotein-cholesterol >2.0 mmol/L despite maximally tolerated statin therapy. During follow-up physicians received online reminders of treatment recommendations of 2009 patients (median age, 63 years, 42% women), 52.4% had CVD only, 31.7% FH only, and 15.9% both CVD and FH. Patients with FH were younger and more likely to be women and non-White with significantly higher baseline low-density lipoprotein-cholesterol level (mmol/L) as compared with patients with CVD (FH 3.92±1.48 versus CVD 2.96±0.94, P <0.0001). Patients with FH received less statin (70.6% versus 79.2%, P =0.0001) at baseline but not ezetimibe (28.1% versus 20.4%, P =0.0003). Among patients with FH only, 45.3% were at low-density lipoprotein target (≥ 50% reduction from pre-treatment level or low-density lipoprotein <2.5 mmol/L) at baseline and increasing to 65.8% and 73.6% by visit 2 and 3, respectively. Among patients with CVD only, none were at recommended level (≤2.0 mmol/L) at baseline and 44.3% and 53.3% were at recommended level on second and third visit, respectively. When primary end point was analyzed as a difference between baseline and last available follow-up observation, only 22.0% of patients with FH only achieved it as compared with 45.8% with CVD only ( P <0.0001) and 55.2% with both FH+CVD ( P <0.0001). Conclusions There is significant treatment inertia in patients with FH including those with CVD. Education focused on patients with FH should continue to be undertaken.

Glucagon-like peptide-1 receptor agonists and sodium-dependent glucose cotransporter-2 inhibitors have demonstrated clinically significant benefits on glycated hemoglobin, weight, blood pressure and cardiorenal outcomes. The emerging evidence from clinical trials and meta-analyses that assessed the combination of these 2 classes of drugs has been promising. An expert forum that included individuals with expertise in endocrine, cardiology and nephrology issues was held in May 2020 to review the literature on the metabolic and cardiorenal benefits of these 2 classes, independently and in combination, in adults with type 2 diabetes mellitus. Although hard outcome data are not available, the group concluded that the combination of glucagon-like peptide-1 receptor agonists with sodium-dependent glucose cotransporter-2 inhibitors is an emerging option for managing adults with type 2 diabetes as long as cost is not a barrier. Ongoing research may offer further insights on hard cardiorenal outcomes for this therapeutic combination as well as provide direction on the potential of this approach in obesity, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis and populations without diabetes., (Copyright © 2020 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)

Spontaneous coronary artery spasm is an important cause of morbidity both in patients with atherosclerotic coronary artery disease and in those with Prinzmetal's angina. Coronary vasospasm tends to occur in focal areas in the coronary tree and can be readily induced by the use of various agents. Spontaneous severe multivessel spasm, mimicking severe obstructive coronary artery disease, has been infrequently described. The therapeutic dilemma in such a clinical situation is highlighted in our current case where an unnecessary coronary artery bypass graft surgery (CABG) was performed due to the lack of clinical suspicion of spasm. This patient presented 5 years after triple-vessel CABG with an episode of rest angina, and was initially found to have severe obstruction of all three native coronary arteries with patent grafts to the right coronary and left anterior descending arteries. After nitroglycerin injection, all three native vessels appeared large and normal. This report raises the question of whether the routine use of intracoronary nitroglycerin, largely abandoned over the past 20 years, should be revisited, at least for certain patient populations such as those with rest angina.

Chronic left ventricular systolic dysfunction is a well recognized problem with an increasingly significant impact on healthcare in the form of congestive heart failure (CHF). Advances in medicine have led to improved survival after myocardial infarction (MI) and as a result, an increased prevalence of left ventricular systolic dysfunction. An increased incidence of thromboembolism, especially stroke, in patients with left ventricular systolic dysfunction is also well recognized. Pharmacological strategies to prevent stroke have been proposed in numerous studies. For example, anticoagulation in patients with atrial fibrillation and heart failure has been shown to reduce mortality rates and the incidence of stroke; however, its role in patients with left ventricular dysfunction and normal sinus rhythm is unclear and utilization of anticoagulation in these patients varies widely. The role of aspirin to prevent thromboembolism in patients with CHF is controversial. The relatively new pharmacological agent ximelagatran, which has an advantage of unmonitored oral administration has the potential to change the anticoagulation strategy in patients with heart failure. Important trials to define optimal therapy for reducing the risk of thromboembolism and death in patients with left ventricular systolic dysfunction and sinus rhythm include the recently reported WATCH (Warfarin and Antiplatelet Therapy in Chronic Heart failure) trial and the WARCEF (Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction) trial, which is currently underway. The WATCH trial failed to outline significant differences between aspirin (acetylsalicylic acid), warfarin, and clopidogrel in the primary composite endpoint of all-cause mortality, nonfatal MI, and nonfatal stroke. Combined data from WATCH and WARCEF may provide sufficient statistical power to clarify outcomes such as stroke and death in patients with reduced cardiac ejection fraction. The pooled data may also help define optimal preventative measures for thromboembolism in patients with left ventricular systolic dysfunction and sinus rhythm.