Differences in provider approach to initiating and titrating guideline directed medical therapy in heart failure with reduced ejection fraction.

BACKGROUND: Despite the strong evidence supporting guideline-directed medical therapy (GDMT) in patients with heart failure with reduced ejection fraction (HFrEF), prescription rates in clinical practice are still lacking. METHODS: A survey containing 20 clinical vignettes of patients with HFrEF was answered by a national sample of 127 cardiologists and 68 internal/family medicine physicians. Each vignette had 4-5 options for adjusting GDMT and the option to make no medication changes. Survey respondents could only select one option. For analysis, responses were dichotomized to the answer of interest. RESULTS: Cardiologists were more likely to make GDMT changes than general medicine physicians (91.8% vs. 82.0%; OR 1.84 [1.07-3.19]; p = 0.020). Cardiologists were more likely to initiate beta-blockers (46.3% vs. 32.0%; OR 2.38 [1.18-4.81], p = 0.016), angiotensin receptor blocker/neprilysin inhibitor (ARNI) (63.8% vs. 48.1%; OR 1.76 [1.01-3.09], p = 0.047), and hydralazine and isosorbide dinitrate (HYD/ISDN) (38.2% vs. 23.7%; OR 2.47 [1.48-4.12], p < 0.001) compared to general medicine physicians. No differences were found in initiating angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEi/ARBs), initiating mineralocorticoid receptor antagonist (MRA), sodium-glucose transporter protein 2 (SGLT2) inhibitors, digoxin, or ivabradine. CONCLUSIONS: Our results demonstrate cardiologists were more likely to adjust GDMT than general medicine physicians. Future focus on improving GDMT prescribing should target providers other than cardiologists to improve care in patients with HFrEF.

Patient self-assessment of urine dipsticks to estimate sodium intake in patients with hypertension.

BACKGROUND & AIMS: Dietary sodium restriction is recommended by current guidelines to reduce blood pressure and decrease the risk of cardiovascular disease. Current methods to assess sodium intake such as dietary questionnaires and 24-h urine collection are cumbersome, and the results are not readily available to patients. In this analysis, we evaluated using chloride and creatinine dipsticks as a convenient method to monitor sodium intake, in addition to patients' ability to practice this method independently. METHODS: This is a post-hoc analysis of a previously published trial, LowSalt4Life, that measured change in sodium consumption over 8 weeks to evaluate the effect of a just-in-time adaptive mobile application intervention. Participants were instructed on how to complete and interpret Quantab® chloride and Multistix® PRO 10 LS creatinine dipstick measurements at home and upload a picture of their results. A pharmacy student interpreted the chloride dipsticks, and intraclass correlation coefficients (ICC) were calculated to assess interrater reliability between the participant and pharmacy student. Predicted 24-h sodium values were calculated by the Kawasaki and Mann methods and compared to actual 24-h sodium excretion. RESULTS: There was a strong interobserver correlation between interpretations of the chloride dipsticks, with the ICC values 0.90, 0.97, 0.99, and 0.98 at weeks 2, 4, 6, and 8, respectively. There was a moderate correlation between the dipstick predicted 24-h sodium excretion and actual 24-h sodium excretion at baseline (r = 0.506; P < 0.001), and a weak correlation at week 8 (r = 0.187; P = 0.217). When corrected creatinine values were used, the dipstick predicted 24-h sodium excretion correlated with the actual 24-h sodium excretion at baseline and week 8 (r = 0.512; P < 0.001 and r = 0.451; P = 0.002). CONCLUSIONS: Our analysis suggests that chloride and creatinine dipsticks have the potential to predict total daily excretion of sodium. This method provides patients with an easy, convenient, and accurate method to assess sodium excretion at home. Further research is needed to identify the optimal timing of performing the dipstick analysis as well as ways to improve the creatinine measurement of the urine samples. TRIAL REGISTRATION: ClinicalTrials.gov NCT03099343; https://clinicaltrials.gov/ct2/show/NCT03099343.

The Role of sGC Stimulators and Activators in Heart Failure With Reduced Ejection Fraction.

Over the past decade, soluble guanylate cyclase (sGC) activators and stimulators have been developed and studied to improve outcomes in patients with heart failure with reduced ejection fraction (HFrEF). The sGC enzyme plays an important role in the nitric oxide (NO)-sGC-cyclic guanosine monophosphate (cGMP) pathway, that has been largely untargeted by current guideline directed medical therapy (GDMT) for HFrEF. Disruption of the NO-sCG-cGMP pathway can be widely observed in patients with HFrEF leading to endothelial dysfunction. The disruption is caused by an oxidized state resulting in low bioavailability of NO and cGMP. The increase in reactive oxygen species can also result in an oxidized, and subsequently heme free, sGC enzyme that NO is unable to activate, furthering the endothelial dysfunction. The novel sGC stimulators enhance the sensitivity of sGC to NO, and independently stimulate sGC, while the sGC activators target the oxidized and heme free sGC to stimulate cGMP production. This review will discuss the pathophysiologic basis for sGC stimulator and activator use in HFrEF, review the pre-clinical and clinical data, and propose a place in the HFrEF armamentarium for this novel pharmacotherapeutic class.