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Background: Ivabradine, a selective sinus node inhibitor, is indicated for patients with chronic heart failure with reduced ejection fraction (HFrEF). Use in cardiogenic shock is currently contraindicated. However, studies have suggested increasing heart rate may be deleterious for patients with HFrEF due to an inverted Bowditch-Treppe response. Limited case series have suggested use of Ivabradine in decompensated HFrEF may be beneficial. We present a case series of patients who presented with severely decompensated HFrEF and received inotropic support and concomitant ivabradine. Methods: We selected four patients with HFrEF presenting with elevated sinus heart rate and cardiogenic shock (cardiac index <2.0L/min*m2with pulmonary artery wedge pressure > 20 mmHg by invasive hemodynamic monitoring) while on inotropic therapy and were intolerant of beta blockade due to hypotension. Ivabradine 2.5 mg 12 h was initiated and subsequently titrated with continued monitoring with baseline, 24 h and latest obtained parameters recorded. Other treatments occurred at the discretion of the attending physician. Results: Four male patients (mean age 44 years) with non-ischemic cardiomyopathy (mean EF 17%, mean NT-pro-BNP 5104 pg/ml) were included. Ivabradine was tolerated in all cases, with a mean dose of 6 mg q12h. Mean heart rate and pulmonary wedge pressure fell 20% and 32% respectively from baseline to last measurement, while stroke volume increased with an overall improvement in cardiac index. (Table 1) There were no changes noted in mean arterial blood pressure. All patients underwent successful wean of inotropic support within 48 hours and were discharged alive on beta blocker and ACE inhibitor therapy. No adverse events attributed to use of Ivabradine were observed. Conclusion: In our small series of patients with cardiogenic shock, beta blocker intolerance and elevated sinus heart rate, Ivabradine was added without any deleterious hemodynamic effect and associated with early clinical improvement. Further studies are needed to better assess its potential use in this population. [ABSTRACT FROM AUTHOR]

Background: In the DAPA-HF trial (Dapagliflozin and Prevention of Adverse-Outcomes in Heart Failure), the sodium-glucose cotransporter 2 inhibitor dapagliflozin reduced the risk of worsening heart failure and death in patients with heart failure and reduced ejection fraction. We examined the efficacy and tolerability of dapagliflozin in relation to background diuretic treatment and change in diuretic therapy after randomization to dapagliflozin or placebo.Methods: We examined the effects of study treatment in the following subgroups: no diuretic and diuretic dose equivalent to furosemide <40, 40, and >40 mg daily at baseline. We examined the primary composite end point of cardiovascular death or a worsening heart failure event and its components, all-cause death and symptoms.Results: Of 4616 analyzable patients, 736 (15.9%) were on no diuretic, 1311 (28.4%) were on <40 mg, 1365 (29.6%) were on 40 mg, and 1204 (26.1%) were taking >40 mg. Compared with placebo, dapagliflozin reduced the risk of the primary end point across each of these subgroups: hazard ratios were 0.57 (95% CI, 0.36-0.92), 0.83 (95% CI, 0.63-1.10), 0.77 (95% CI, 0.60-0.99), and 0.78 (95% CI, 0.63-0.97), respectively (P for interaction=0.61). The hazard ratio in patients taking any diuretic was 0.78 (95% CI, 0.68-0.90). Improvements in symptoms and treatment toleration were consistent across the diuretic subgroups. Diuretic dose did not change in most patients during follow-up, and mean diuretic dose did not differ between the dapagliflozin and placebo groups after randomization.Conclusions: The efficacy and safety of dapagliflozin were consistent across the diuretic subgroups examined in DAPA-HF. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03036124. [ABSTRACT FROM AUTHOR]