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BACKGROUND In patients with type 2 diabetes, inhibitors of sodium-glucose cotransporter 2 (SGLT2) reduce the risk of a first hospitalization for heart failure, possibly through glucoseindependent mechanisms. More data are needed regarding the effects of SGLT2 inhibitors in patients with established heart failure and a reduced ejection fraction, regardless of the presence or absence of type 2 diabetes. METHODS In this phase 3, placebo-controlled trial, we randomly assigned 4744 patients with New York Heart Association class II, III, or IV heart failure and an ejection fraction of 40% or less to receive either dapagliflozin (at a dose of 10 mg once daily) or placebo, in addition to recommended therapy. The primary outcome was a composite of worsening heart failure (hospitalization or an urgent visit resulting in intravenous therapy for heart failure) or cardiovascular death. RESULTS Over a median of 18.2 months, the primary outcome occurred in 386 of 2373 patients (16.3%) in the dapagliflozin group and in 502 of 2371 patients (21.2%) in the placebo group (hazard ratio, 0.74; 95% confidence interval [CI], 0.65 to 0.85; P<0.001). A first worsening heart failure event occurred in 237 patients (10.0%) in the dapagliflozin group and in 326 patients (13.7%) in the placebo group (hazard ratio, 0.70; 95% CI, 0.59 to 0.83). Death from cardiovascular causes occurred in 227 patients (9.6%) in the dapagliflozin group and in 273 patients (11.5%) in the placebo group (hazard ratio, 0.82; 95% CI, 0.69 to 0.98); 276 patients (11.6%) and 329 patients (13.9%), respectively, died from any cause (hazard ratio, 0.83; 95% CI, 0.71 to 0.97). Findings in patients with diabetes were similar to those in patients without diabetes. The frequency of adverse events related to volume depletion, renal dysfunction, and hypoglycemia did not differ between treatment groups. CONCLUSIONS Among patients with heart failure and a reduced ejection fraction, the risk of worsening heart failure or death from cardiovascular causes was lower among those who received dapagliflozin than among those who received placebo, regardless of the presence or absence of diabetes. (Funded by AstraZeneca; DAPA-HF ClinicalTrials .gov number, NCT03036124.

S pe c i a l R e p o r tT h e ne w e ngl a nd jou r na l o f m e dicine n engl j med nejm.org T h e ne w e ngl a nd jou r na l o f m e dicine n engl j med nejm.org

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oronaviruses (CoVs) are single-stranded positive-sense RNA viruses, with the capacity for rapid mutation and recombination. Coronaviruses are known to cause respiratory or intestinal infections in humans and animals. 1 Acute respiratory infections, including influenza, respiratory syncytial virus, and bacterial pneumonias, are well-recognized triggers for cardiovascular diseases (CVD), 2,3 and the underlying CVD is usually associated with comorbidities, which may increase the incidence and severity of infectious diseases. 4 The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, which causes coronavirus disease 2019 (COVID-19), has rapidly grown into a pandemic, and a large proportion of affected patients have been reported to have underlying CVD. 5,6 In this report, we briefly review the basics of coronaviruses and their potential effects on the cardiovascular system. Our knowledge of COVID-19 is still evolving rapidly, and this review discusses previous learnings from outbreaks of SARS and Middle East respiratory syndrome (MERS), as well as seasonal influenza, to obtain further insight into effects of coronaviruses on the cardiovascular system. Understanding the effects of COVID-19 on the cardiovascular system is essential for providing comprehensive medical care for cardiac patients. Coronaviruses in HumansCoronaviruses are named for crownlike spikes on their surface and belong to the Coronavirinae subfamily, which are further classified into 4 groups: the α, β, γ, and δ CoVs by phylogenetic clustering, of which α and β are known to cause infection in humans. 7 Coronaviruses contain 4 major structural proteins: the spike (S) protein (which mediates attachment to the host receptor and subsequent fusion of the virus and cell membrane), the nucleocapsid (N) protein, the membrane (M) protein, and the envelope (E) protein. 8 The first human CoV (HCoV) was identified in the mid-1960s in human embryonic tracheal organ cultures, and until 2003, only 2 HCoV species, HCoV-229E and HCoV-OC43, were recognized. Currently, 7 different CoV strains are known to infect humans, including HCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1, which generally cause self-resolving infection. There are also severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East Respiratory Syndrome coronavirus (MERS-CoV), and newly identified SARS-CoV-2, which can cause lethal respiratory infections in humans. 9,10 IMPORTANCE Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19) has reached a pandemic level. Coronaviruses are known to affect the cardiovascular system. We review the basics of coronaviruses, with a focus on COVID-19, along with their effects on the cardiovascular system.OBSERVATIONS Coronavirus disease 2019 can cause a viral pneumonia with additional extrapulmonary manifestations and complications. A large proportion of patients have underlying cardiovascular disease and/or cardiac risk factors. Factors associated with mortality include mal...

In this trial, patisiran improved multiple clinical manifestations of hereditary transthyretin amyloidosis. (Funded by Alnylam Pharmaceuticals; APOLLO ClinicalTrials.gov number, NCT01960348 .).

In patients with heart failure and a preserved ejection fraction, treatment with spironolactone did not significantly reduce the incidence of the primary composite outcome of death from cardiovascular causes, aborted cardiac arrest, or hospitalization for the management of heart failure. (Funded by the National Heart, Lung, and Blood Institute; TOPCAT ClinicalTrials.gov number, NCT00094302.).