Heart Failure

Introduction

In the first world nation like Europe and the U.S., heart failure remains a massive challenge for medical practitioners. It accounts for approximately a million hospitalizations each year in the two continents (Ambrosy et al., 2014). However, it is important to underscore the reductions in morbidity and mortality from heart failure with the introduction of successive generations of evidence based medication as well as device therapies. As Sacks et al. (2014) provide, numerous medical publications detailing randomized and controlled trials for various heart failure treatments offer insights to the progress realized since 1986. The article titled Foundations of pharmacotherapy for heart failure with reduced ejection fraction: evidence meets practice, part II by details trials on a relatively new treatment (Mcllvenan & Page II 2016).It is recommended by the American College of Cardiology Foundation (ACCF) and American Heart Association (AHA) 2013 Guidelines for the Management of Heart Failure.

Summary

Heart failure affects patients in different ways. One category is the heart failure reduced ejection fraction (HFrEF) while the other is heart failure with preserved ejection fraction (HFpEF) (Mcllvenan & Page II 2016). Clinical trials are thus conducted in two separate ways towards determining which treatment regimens avail the bet efficacy results. The article by Mcllvenan and Page II (2016) offers descriptions of pharmacological agents mentioned in the 2013 Guidelines for the Management of Heart failure with respect to HFrEF. These agents include β-Adrenergic antagonists, Digoxin, and Aldosterone antagonists.

In all cases, β-blockers like Propranolol, Metoprolol, Bisoprolol, Carvedilol, and Nebivolol are employed in first line treatment for HF patients. For the first generation of these medications, clinical trials indicated that Propranolol worsened symptoms (Mcllvenan & Page II 2016). Persistent research allowed for evidence oriented introduction of Metoprolol which achieved admirable results in accordance with the results from subsequent clinical trials. Bisoprolol trials similarly indicated the achievement of fewer hospitalizations and enhanced functional status. In 2001, Carvedilol clinical trials indicated that it resulted in mortality rates lower by 17% compared to metoprolol and its variants (Mcllvenan & Page II 2016). With regard to Digoxin, clinical trials spanning the US and Canada indicated negligible difference relative to reduction of cardio-vascular mortality rates among patients involved in the endeavors (Mcllvenan & Page II 2016). However, in comparison with the placebo group, the drug exhibited notable strengths in diminishing hospitalizations for HFrEF patients. On the other hand, Aldosterone antagonists have thus gained evidence based recommendations for reducing chances of morbidity and mortality among patients with 40% lVEF and suffered a recent acute myocardial infarction. Aldosterone antagonists trials, results provided that these class of medications reduced sudden cardiac arrest fatalities, low HF progression rates, and lesser hospitalizations.

β-Adrenergic antagonists seek to correct the down-regulation occurring among HFrEF patients which allows for β₂ receptors to become dominant as β₁ receptors are undermined by catecholamines. The outcome is the release of a cardiomyopathy phenotype and systolic dysfunction. α₁ receptors present in the myocardium also result in concentric hypertrophy leading to continuous and excessive adrenergic drive in patients with HFrEF (Mcllvenan & Page II 2016). β blockers serve to limit such devastating impacts on cardiac myocytes due to β and α adrenergic receptors. Thus, patients are able to experience improved systolic functioning, acceptable heart rate, reduced ventricular and atrial arrhythmias, limited remodeling progression, as well as anti-ischemic effects.

The pathophysiological mechanisms associated with Digoxin revolve about its capacity to obstruct α sodium-potassium ATPase subunits found on myocyte membranes. The result is an accumulation of intercellular sodium which conversely allows for calcium availability thus improving myocardial contraction forces (Mcllvenan & Page II 2016). For Aldosterone Antagonists, it is known that plasma aldosterone concentration is notably higher in HFrEF patients thereby increasing mortality risk and HF severity. Treatments are therefore designed to inhibit aldosterone production in a number of sites like in the spironolactone and eplerenone receptor areas.

Conclusion

As availed by the American College of Cardiology Foundation (ACCF) and American Heart Association (AHA) 2013 Guidelines for the Management of Heart Failure, the three classes of HFrEF treatment are supported with robust clinical trials. For β-blockers consistency in research enabled researchers to dismiss Propranolol and continue with developments which have led to the introduction of Metoprolol, Bisoprolol, Carvedilol, and Nebivolol. Trials on Digoxin show that its effects to improving HFrEF patient outcome are weaker in comparison to β-blockers and aldosterone antagonists.

References

Ambrosy, A. P., Fonarow, G. C., Butler, J., Chioncel, O., Greene, S. J., Vaduganathan, M., … & Gheorghiade, M. (2014). The global health and economic burden of hospitalizations for heart failure: lessons learned from hospitalized heart failure registries. Journal of the American College of Cardiology, 63(12), 1123-1133.

McIlvennan, C. K., & Page, R. L. (2016). Foundations of Pharmacotherapy for Heart Failure With Reduced Ejection Fraction: Evidence Meets Practice, Part II. Journal of Cardiovascular Nursing, 31(6), 545-554.

Sacks, C. A., Jarcho, J. A., & Curfman, G. D. (2014). Paradigm shifts in heart-failure therapy—a timeline. New England Journal of Medicine, 371(11), 989-991.