Coronavirus disease 2019 (COVID-19) is a global pandemic affecting 185 countries and >3 000 000 patients worldwide as of April 28, 2020. COVID-19 is caused by severe acute respiratory syndrome coronavirus 2, which invades cells through the angiotensin-converting enzyme 2 receptor. Among patients with COVID-19, there is a high prevalence of cardiovascular disease, and >7% of patients experience myocardial injury from the infection (22% of critically ill patients). Although angiotensin-converting enzyme 2 serves as the portal for infection, the role of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers requires further investigation. COVID-19 poses a challenge for heart transplantation, affecting donor selection, immunosuppression, and posttransplant management. There are a number of promising therapies under active investigation to treat and prevent COVID-19.

Objective: To study whether combining vital signs and electrocardiogram (ECG) analysis can improve early prognostication. Methods: This study analyzed 1258 adults with coronavirus disease 2019 who were seen at three hospitals in New York in March and April 2020. Electrocardiograms at presentation to the emergency department were systematically read by electrophysiologists. The primary outcome was a composite of mechanical ventilation or death 48 hours from diagnosis. The prognostic value of ECG abnormalities was assessed in a model adjusted for demographics, comorbidities, and vital signs. Results: At 48 hours, 73 of 1258 patients (5.8%) had died and 174 of 1258 (13.8%) were alive but receiving mechanical ventilation with 277 of 1258 (22.0%) patients dying by 30 days. Early development of respiratory failure was common, with 53% of all intubations occurring within 48 hours of presentation. In a multivariable logistic regression, atrial fibrillation/flutter (odds ratio [OR], 2.5; 95% CI, 1.1 to 6.2), right ventricular strain (OR, 2.7; 95% CI, 1.3 to 6.1), and ST segment abnormalities (OR, 2.4; 95% CI, 1.5 to 3.8) were associated with death or mechanical ventilation at 48 hours. In 108 patients without these ECG abnormalities and with normal respiratory vitals (rate <20 breaths/min and saturation >95%), only 5 (4.6%) died or required mechanical ventilation by 48 hours versus 68 of 216 patients (31.5%) having both ECG and respiratory vital sign abnormalities. Conclusion: The combination of abnormal respiratory vital signs and ECG findings of atrial fibrillation/flutter, right ventricular strain, or ST segment abnormalities accurately prognosticates early deterioration in patients with coronavirus disease 2019 and may assist with patient triage.

Aims Left ventricular assist device (LVAD) therapy improves the haemodynamics of advanced heart failure patients. However, it is unknown whether haemodynamic optimization improves haemocompatibility‐related adverse events (HRAEs). This study aimed to assess HRAEs in patients with optimized haemodynamics. Methods and results Eighty‐three outpatients [aged 61 (53–67) years, 50 male] underwent a haemodynamic ramp test at 253 (95–652) days after LVAD implantation, and 51 (61%) had optimized haemodynamics (defined as central venous pressure < 12 mmHg, pulmonary artery wedge pressure < 18 mmHg, cardiac index > 2.2 L/min/m2) following LVAD speed adjustment. One‐year survival free of any HRAEs (non‐surgical bleeding, thromboembolic event, pump thrombosis, or neurological event) was achieved in 75% of the optimized group and in 44% of the non‐optimized group (hazard ratio 0.36, 95% confidence interval 0.18–0.73, P = 0.003). The net haemocompatibility score, using four escalating tiers of hierarchal severity to derive a total score for events, was significantly lower in the optimized group than the non‐optimized group (1.02 vs. 2.00 points/patient; incidence rate ratio 0.51, 95% confidence interval 0.29–0.90, P = 0.021). Conclusion Left ventricular assist device patients in whom haemodynamics can be optimized had greater freedom from HRAEs compared to those without optimized haemodynamics.

BACKGROUND: Left ventricular assist device (LVAD) therapy improves the hemodynamics of advanced heart failure patients. However, it is unknown whether hemodynamic optimization improves clinical outcomes. The aim of this study was to investigate whether hemodynamic optimization reduces hospital readmission rate in LVAD patients. METHODS AND RESULTS: LVAD patients undergoing an invasive hemodynamic ramp test were prospectively enrolled and followed for 1 year. LVAD speed was optimized using a ramp test, targeting the following goals: central venous pressure <12 mm Hg, pulmonary capillary wedge pressure <18 mm Hg, and cardiac index >2.2 L/(min•m 2). The frequency and cause of hospital readmissions were compared between patients who achieved (optimized group) or did not achieve (nonoptimized group) these goals. Eighty-eight outpatients (median 61 years old, 53 male) underwent ramp testing 236 days after LVAD implantation, and 54 (61%) had optimized hemodynamics after LVAD speed adjustment. One-year survival after the ramp study was comparable in both groups (89% versus 88%). The total hospital readmission rate was lower in the optimized group compared with the nonoptimized group (1.15 versus 2.86 events/y, P<0.001). This result was predominantly because of a reduction in the heart failure readmission rate in the optimized group (0.08 versus 0.71 events/y, P=0.016). CONCLUSIONS: LVAD patients, in whom hemodynamics were optimized, had a significantly lower rate of hospital readmissions, primarily because of fewer heart failure admissions. These findings highlight the importance of achieving hemodynamic optimization in LVAD patients.

Background: Hemodynamic ramp (HR) tests can guide the optimization of left ventricular assist device (LVAD) speed and direct medical therapy. We investigated the effects of HR-guided LVAD management. Methods and Results: This prospective, multicenter, randomized, pilot study compared outcomes in LVAD patients using an HR-guided (HR group) versus a standard transthoracic echocardiography-guided (control group) management strategy. Patients were enrolled and randomized 1 to 3 months post-HVAD implantation and followed for 6 months. Twenty-two patients (57±10 years, 73% male) were randomized to the HR group and 19 patients (51±13 years, 63% male) to the control group. HR group patients had double the number of LVAD speed changes (1.68 versus 0.84 changes/patient, P =0.09 with an incidence rate ratio 2.0, 95% CI, 0.9–4.7) with twice the magnitude of rotations per minute changes (130 versus 60 rotations per minute/patient, P =0.004) during the study. The HR group also had 2-fold greater heart failure medication changes (4.32 versus 2.53 changes/patient, P =0.072, incidence rate ratio 1.7 with 95% CI, 0.8–3.5) predominantly because of changes in diuretic dose (40 versus 0 mg/patient, P <0.001). The HR group had numerically but not statistically higher event-free survival (62% versus 46%, P =0.087; hazard ratio, 0.46 with 95% CI, 0.2–1.2), with numerically but not statistically lower events per patient-year ( P =0.084). There were no significant differences in the 6-minute walk or Kansas City Cardiomyopathy Questionnaire tests at 6 months. Conclusions: In this randomized pilot study of LVAD patient management we demonstrated the feasibility of standardized HR testing at multiple institutions and that a strategy guided by hemodynamics was associated with more LVAD speed and medication adjustments and a nonsignificant reduction in adverse events. A pivotal study to demonstrate the clinical benefit of HR testing is warranted. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03021239.