Prognostic markers in heart failure—congestion, neurohormones, and the cardiorenal syndrome

Abstract

There are several markers of poor prognosis in heart failure (HF). The most established markers of poor prognosis in HF include neurohormonal (NH) imbalance, low ejection fraction (EF), ventricular arrhythmias, intraventricular conduction delays, low functional capacity, low SBP, and renal failure. The relative importance of these factors is unknown, as they have never been studied together. We present a 74-year-old female with nonischemic cardiomyopathy and an EF<20% who over 24 years since diagnosis, never developed clinical or hemodynamic congestion, was never hospitalized for HF, and never required a loop diuretic. She had all of the clinical indicators of poor prognosis in HF except for severe NH imbalance and renal failure, illustrating their importance in HF prognosis. While NH activation in HF is initially an adaptive mechanism, an imbalance of NH effectors causes congestion leading to a vicious cycle of congestion, renal dysfunction, and worsening of HF. The combination of NH activation and renal failure in HF is a vasomotor nephropathy known as the cardiorenal syndrome (CRS) and portends a poor prognosis. Pharmacological disruption of NH pathways early in HF may prevent CRS and, therefore, improve outcomes.

Short and long-term effects of continuous versus intermittent loop diuretics treatment in acute heart failure with renal dysfunction

“…Moreover, the exact role of impaired renal function during hospitalization is currently under debate: some authors consider it as an important target and prognostic indicator, while others believe it is merely the final equivalent of systemic hemodynamic and neuroendocrine unbalance [14][15][16]. In our sample, worsening renal function during the hospitalization period seemed to have less clinical impact compared to the post discharge period.…”

Endothelial Dysfunction, Arterial Stiffness, and Heart Failure

“…Increasing HF severity is associated with NO imbalance and endothelial dysfunction that manifests in different forms (52,53). Besides increasing afterload due to systemic (55) and pulmonary vascular constriction (56,57), altered endothelial function underlies regional vasomotor dysregulation in the renal (58) and coronary circulation (59). Decreased coronary endothelium-dependent vasodilator capacity impairs myocardial perfusion, reduces coronary flow (60,61), and worsens ventricular function (53).…”

“…Renal dysfunction. NO imbalance drives vasomotor nephropathy, which underlies acute renal damage and the cardiorenal syndrome in HF (58,87). This action is in part due to reduced renal flow from inappropriate arteriolar vasoconstriction superimposed on baseline low cardiac output.…”

Noninvasive Assessment of Endothelial Function: The Classic Methods and the New Peripheral Arterial Tonometry

“…Within this construct, myocardial adverse effects and endothelial dysfunction related to oxidative stress represent a unifying feature that drives the symptoms and unfavorable outcomes associated with both ischemic and nonischemic HF. Increasing vascular resistance, microvascular dysfunction is responsible of peripheral mechanisms undergoing progression of HF syndrome, by involving renal, 103 pulmonary, 104 and coronary circulation. 97 Importantly, severity of endothelial dysfunction is also related to exercise capacity.…”