Jonathan D. Rich

Continuous-flow ventricular assist device (cfVAD) performance and patient hemodynamic conditions are intimately interrelated and dynamic, changing frequently with alterations in physiologic conditions, particularly pre- and afterloading conditions. The Heartware cfVAD (HVAD) provides a unique feature among currently approved VADs of providing an estimated instantaneous flow waveform, the characteristics of which can provide significant insights into patient and device properties. Despite being readily available, HVAD waveforms are poorly understood, underutilized, and insufficiently leveraged, even by clinicians who regularly manage HVAD patients. The purpose of this review is to provide the theoretical foundation for understanding the determinants of HVAD waveform characteristics and to provide practical examples illustrating how to interpret and integrate changes of HVAD waveforms into clinical practice. Heartware cfVAD waveforms should be considered a complimentary tool for the optimization of medical therapies and device speed in HVAD patients.

Summary: Aims: Sequential nephron blockade with thiazide‐like diuretics is a strategy used to overcome diuretic resistance in acute decompensated heart failure (ADHF), but head‐to‐head studies are lacking and equipoise exists regarding the preferred thiazide‐like diuretic in this setting. We thus compared the effectiveness of oral metolazone versus intravenous (IV) chlorothiazide as add‐on therapy to loop diuretics in hospitalized patients with ADHF and renal dysfunction.Methods: This retrospective cohort study evaluated the efficacy and safety of oral metolazone versus IV chlorothiazide as add‐on therapy to loop diuretics in patients hospitalized with ADHF and renal dysfunction. The primary endpoint was net urine output (UOP) at 72 h after initiation of thiazide‐like diuretics. Safety endpoints included worsening renal function, hypotension, and electrolyte abnormalities.Results: Fifty‐five patients were enrolled with 33 patients receiving metolazone and 22 patients receiving chlorothiazide. There was no difference in median net UOP at 72 h in those receiving metolazone (4828 mL, interquartile range [IQR] 2800–7209 mL) compared to chlorothiazide (3779 mL, IQR 1885–6535 mL) (P = 0.16). There was no difference in hypotension, worsening renal function, hyponatremia, or hypokalemia (P = NS for all comparisons). Hospital length of stay was shorter in the metolazone cohort (median 7 days) compared to chlorothiazide (median 15 days), suggesting the chlorothiazide cohort was likely sicker.Conclusion: Sequential nephron blockade with either metolazone or chlorothiazide appears to be efficacious and safe in ADHF, renal dysfunction, and diuretic resistance. Given the considerable cost difference favoring oral metolazone, larger randomized studies are warranted to confirm our findings and to exclude the possibility of confounding by indication.

The Third International Right Heart Failure Summit (Boston, MA) convened a group of international clinical and scientific experts in pulmonary vascular disease and right heart disease to explore cutting‐edge developments in the mechanisms and clinical management of right‐sided cardiovascular disease. The symposium was organized into three distinct sessions, the first of which was titled “Pulmonary Hypertension and the Right Ventricle—Thinking outside the Box” and will be the focus of this review. Three internationally renowned experts in pulmonary hypertension and right heart disease—Drs. Stuart Rich, Sean Gaine, and Harm Bogaard—each delivered provocative lectures. The first lecture, by Dr. Rich, was titled “Current Classification for Pulmonary Hypertension—Why Are We Ignoring the Structural Basis of the Disease?” Rich focused on the current classification system of pulmonary hypertension and provided a unique historical perspective. He also addressed the need to evolve the prevailing conceptual framework of our approach to pulmonary vascular diseases and right ventricular dysfunction, including the future design of pulmonary hypertension clinical trials. Dr. Gaine delivered the second lecture, titled “Treatment Algorithm for Pulmonary Hypertension: Tunnel Vision of our Current Approach.” Gaine emphasized the tripartite model of pulmonary hypertension management, namely, supportive measures, pharmacologic therapy, and rescue therapy. Specifically, he detailed how each of these entities is changing as our understanding of the unmet needs in the field of pulmonary hypertension is becoming increasingly apparent. Finally, Dr. Bogaard provided a lecture titled “Treating Right Heart Failure: Why Does the Art of Medicine Lead the Science?” Bogaard provided a stimulating review of cutting‐edge translational research of right ventricular function and dysfunction. In particular, he described a variety of molecular and cellular changes that occur in the hypertrophied right ventricle and contrasted those changes that may be adaptive from those that are maladaptive and may be potential therapeutic targets.