Cardiology

Michelena, H. I., A. Della Corte, A. Evangelista, J. J. Maleszewski, W. D. Edwards, M. J. Roman, R. B. Devereux, B. Fernández, F. M. Asch, A. J. Barker, L. M. Sierra-Galan, L. De Kerchove, S. M. Fernandes, P. W. M. Fedak, E. Girdauskas, V. Delgado, S. Abbara, E. Lansac, S. K. Prakash, M. M. Bissell, B. A. Popescu, M. D. Hope, M. Sitges, V. H. Thourani, P. Pibarot, K. Chandrasekaran, P. Lancellotti, M. A. Borger, J. K. Forrest, J. Webb, D. M. Milewicz, R. Makkar, M. B. Leon, S. P. Sanders, M. Markl, V. A. Ferrari, W. C. Roberts, J. K. Song, P. Blanke, C. S. White, S. Siu, L. G. Svensson, A. C. Braverman, J. Bavaria, T. M. Sundt, G. E. Khoury, R. De Paulis, M. Enriquez-Sarano, J. J. Bax, C. M. Otto and H. J. Schäfers (2021). “Summary: International consensus statement on nomenclature and classification of the congenital bicuspid aortic valve and its aortopathy, for clinical, surgical, interventional, and research purposes.” J Thorac Cardiovasc Surg 162(3): 781-797.

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This International evidence-based nomenclature and classification consensus on the congenital bicuspid aortic valve and its aortopathy recognizes 3 types of bicuspid aortic valve: 1. Fused type, with 3 phenotypes: right-left cusp fusion, right-non cusp fusion and left-non cusp fusion; 2. 2-sinus type with 2 phenotypes: Latero-lateral and antero-posterior; and 3. Partial-fusion or forme fruste. This consensus recognizes 3 bicuspid-aortopathy types: 1. Ascending phenotype; root phenotype; and 3. extended phenotypes.

Michelena, H. I., A. Della Corte, A. Evangelista, J. J. Maleszewski, W. D. Edwards, M. J. Roman, R. B. Devereux, B. Fernández, F. M. Asch, A. J. Barker, L. M. Sierra-Galan, L. De Kerchove, S. M. Fernandes, P. W. M. Fedak, E. Girdauskas, V. Delgado, S. Abbara, E. Lansac, S. K. Prakash, M. M. Bissell, B. A. Popescu, M. D. Hope, M. Sitges, V. H. Thourani, P. Pibarot, K. Chandrasekaran, P. Lancellotti, M. A. Borger, J. K. Forrest, J. Webb, D. M. Milewicz, R. Makkar, M. B. Leon, S. P. Sanders, M. Markl, V. A. Ferrari, W. C. Roberts, J. K. Song, P. Blanke, C. S. White, S. Siu, L. G. Svensson, A. C. Braverman, J. Bavaria, T. M. Sundt, G. El Khoury, R. De Paulis, M. Enriquez-Sarano, J. J. Bax, C. M. Otto and H. J. Schäfers (2021). “Summary: International Consensus Statement on Nomenclature and Classification of the Congenital Bicuspid Aortic Valve and Its Aortopathy, for Clinical, Surgical, Interventional and Research Purposes.” Ann Thorac Surg 112(3): 1005-1022.

Full text of this article.

This International evidence-based nomenclature and classification consensus on the congenital bicuspid aortic valve and its aortopathy recognizes 3 types of bicuspid aortic valve: 1. Fused type, with 3 phenotypes: right-left cusp fusion, right-non cusp fusion and left-non cusp fusion; 2. 2-sinus type with 2 phenotypes: Latero-lateral and antero-posterior; and 3. Partial-fusion or forme fruste. This consensus recognizes 3 bicuspid-aortopathy types: 1. Ascending phenotype; root phenotype; and 3. extended phenotypes.

Michelena, H. I., A. D. Corte, A. Evangelista, J. J. Maleszewski, W. D. Edwards, M. J. Roman, R. B. Devereux, B. Fernández, F. M. Asch, A. J. Barker, L. M. Sierra-Galan, L. De Kerchove, S. M. Fernandes, P. W. M. Fedak, E. Girdauskas, V. Delgado, S. Abbara, E. Lansac, S. K. Prakash, M. M. Bissell, B. A. Popescu, M. D. Hope, M. Sitges, V. H. Thourani, P. Pibarot, K. Chandrasekaran, P. Lancellotti, M. A. Borger, J. K. Forrest, J. Webb, D. M. Milewicz, R. Makkaar, M. B. Leon, S. P. Sanders, M. Markl, V. A. Ferrari, W. C. Roberts, J. K. Song, P. Blanke, C. S. White, S. Siu, L. G. Svensson, A. C. Braverman, J. Bavaria, T. M. Sundt, G. El Khoury, R. De Paulis, M. Enriquez-Sarano, J. J. Bax, C. M. Otto and H. J. Schäfers (2021). “International Consensus Statement on Nomenclature and Classification of the Congenital Bicuspid Aortic Valve and Its Aortopathy, for Clinical, Surgical, Interventional and Research Purposes.” Radiol Cardiothorac Imaging 3(4): e200496.

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This International Consensus Classification and Nomenclature for the congenital bicuspid aortic valve condition recognizes 3 types of bicuspid valves: 1. The fused type (right-left cusp fusion, right-non-coronary cusp fusion and left-non-coronary cusp fusion phenotypes); 2. The 2-sinus type (latero-lateral and antero-posterior phenotypes); and 3. The partial-fusion (forme fruste) type. The presence of raphe and the symmetry of the fused type phenotypes are critical aspects to describe. The International Consensus also recognizes 3 types of bicuspid valve-associated aortopathy: 1. The ascending phenotype; 2. The root phenotype; and 3. Extended phenotypes.

Pocock, S. J., J. P. Ferreira, J. Gregson, S. D. Anker, J. Butler, G. Filippatos, N. D. Gollop, T. Iwata, M. Brueckmann, J. L. Januzzi, A. A. Voors, F. Zannad and M. Packer (2021). “Novel biomarker-driven prognostic models to predict morbidity and mortality in chronic heart failure: the EMPEROR-Reduced trial.” Eur Heart J Aug 23;ehab579. [Epub ahead of print].

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AIMS: The aim of this study was to generate a biomarker-driven prognostic tool for patients with chronic HFrEF. Circulating levels of N-terminal pro B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin T (hs-cTnT) each have a marked positive relationship with adverse outcomes in heart failure with reduced ejection fraction (HFrEF). A risk model incorporating biomarkers and clinical variables has not been validated in contemporary heart failure (HF) trials. METHODS AND RESULTS: In EMPEROR-Reduced, 33 candidate variables were pre-selected. Multivariable Cox regression models were developed using stepwise selection for: (i) the primary composite outcome of HF hospitalization or cardiovascular death, (ii) all-cause death, and (iii) cardiovascular mortality. A total of 3730 patients were followed up for a median of 16 months, 823 (22%) patients had a primary outcome and 515 (14%) patients died, of whom 389 (10%) died from a cardiovascular cause. NT-proBNP and hs-cTnT were the dominant predictors of the primary outcome, and in addition, a shorter time since last HF hospitalization, longer time since HF diagnosis, lower systolic blood pressure, New York Heart Association (NYHA) Class III or IV, higher heart rate and peripheral oedema were key predictors (eight variables in total, all P < 0.001). The primary outcome risk score discriminated well (c-statistic = 0.73), with patients in the top 10th of risk having an event rate >9 times higher than those in the bottom 10th. Empagliflozin benefitted patients across risk levels for the primary outcome. NT-proBNP and hs-cTnT were also the dominant predictors of all-cause and cardiovascular mortality, followed by NYHA Class III or IV and ischaemic aetiology (four variables in total, all P < 0.001). The mortality risk model presented good event discrimination for all-cause and cardiovascular mortality (c-statistic = 0.69 for both). These simple models were externally validated in the BIOSTAT-CHF study, achieving similar c-statistics. CONCLUSIONS: The combination of NT-proBNP and hs-cTnT with a small number of readily available clinical variables provides prognostic assessment for patients with HFrEF. This predictive tool kit can be easily implemented for routine clinical use.

Packer, M., J. Butler, F. Zannad, G. Filippatos, J. P. Ferreira, S. J. Pocock, P. Carson, I. Anand, W. Doehner, M. Haass, M. Komajda, A. Miller, S. Pehrson, J. R. Teerlink, S. Schnaidt, C. Zeller, J. M. Schnee and S. D. Anker (2021). “Effect of Empagliflozin on Worsening Heart Failure Events in Patients with Heart Failure and a Preserved Ejection Fraction: The EMPEROR-Preserved Trial.” Circulation.

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Background: Empagliflozin reduces the risk of cardiovascular death or hospitalization for heart failure in patients with heart failure and a preserved ejection fraction, but additional data are needed about its effect on inpatient and outpatient heart failure events. Methods: We randomly assigned 5988 patients with class II-IV heart failure with an ejection fraction of >40% to double-blind treatment with placebo or empagliflozin (10 mg once daily), in addition to usual therapy, for a median of 26 months. We prospectively collected information on inpatient and outpatient events reflecting worsening heart failure and prespecified their analysis in individual and composite endpoints. Results: Empagliflozin reduced the combined risk of cardiovascular death, hospitalization for heart failure or an emergent/urgent heart failure visit requiring intravenous treatment (432 vs 546 patients; empagliflozin vs placebo, respectively; hazard ratio 0.77, 95% CI: 0.67-0.87), P <0.0001. This benefit reached statistical significance at 18 days after randomization. Empagliflozin reduced the total number of heart failure hospitalizations that required intensive care (hazard ratio 0.71, 95% CI 0.52-0.96, P=0.028) and the total number of all hospitalizations that required a vasopressor or positive inotropic drug (hazard ratio 0.73, 95% CI: 0.55-0.97,P=0.033). As compared with placebo, fewer patients in the empagliflozin group reported outpatient intensification of diuretics (482 vs 610, hazard ratio 0.76, 95% CI: 0.67-0.86, P<0.0001), and patients assigned to empagliflozin were 20-50% more likely to have a better NYHA functional class, with significant effects at 12 weeks that were maintained for at least 2 years. The benefit on total heart failure hospitalizations was similar in patients with an ejection fraction of >40-<50% and 50-<60%, but was attenuated at higher ejection fractions. Conclusions: In patients with heart failure and a preserved ejection fraction, empagliflozin produced a meaningful, early and sustained reduction in the risk and severity of a broad range of inpatient and outpatient worsening heart failure events. Clinical Trial Registration: The registration identifier at ClinicalTrials.gov is NCT03057977.