Cardiology

Packer, M. (2017). “Why is the use of digitalis withering? Another reason that we need medical heart failure specialists.” Eur J Heart Fail: 2017 Oct [Epub ahead of print].

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Contrary to popular opinion, William Withering did not discover digitalis nor was he the first to describe its use for heart failure. In 1785, the esteemed English botanist and physician wrote a pamphlet that summarized his experiences in 163 patients with dropsy. Yet, at the time, digitalis had been known to exert important pharmacological effects for 2000 years. In the first century, the Greek physician, Pedanius Dioscorides, noted the use of digitalis as a therapeutic agent; its application to heart failure was first recorded in print by Leonard Fuchs in 1542.1 Nevertheless, Withering was the first to systematically carry out clinical studies with the plant in a scientific manner, eliminating the superstition that had long surrounded it. Withering’s work was ground-breaking, not because of what he discovered, but how he approached its evaluation. It was the first use of the scientific method for the characterization of a pharmaceutical.

Roberts, W. C. (2017). “Cholesterol is the cause of atherosclerosis.” Am J Cardiol 120(9): 1696.

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Although some investigators have considered cholesterol the cause of atherosclerosis for several decades,1–15 26 authors, mainly from Europe, in April 2017, published an article titled “Low-density lipoproteins cause atherosclerotic cardiovascular disease…,” a consensus statement from the European Atherosclerosis Society Consensus Panel.16 I was glad to see the article that soundly supports the view that cholesterol is the cause of atherosclerosis. Although I found the article unnecessarily difficult, the message is loud and clear. So when your physician recommends a statin drug or ezetimibe or one of the PCSK-9 inhibitors, take it. These drugs are safer than almost any drug one can put in his/her mouth.

Packer, M. (2017). “Activation and inhibition of sodium-hydrogen exchanger is a mechanism that links the pathophysiology and treatment of diabetes mellitus with that of heart failure.” Circulation 136(16): 1548-1559.

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The mechanisms underlying the progression of diabetes mellitus and heart failure are closely intertwined, such that worsening of one condition is frequently accompanied by worsening of the other; the degree of clinical acceleration is marked when the 2 coexist. Activation of the sodium-hydrogen exchanger in the heart and vasculature (NHE1 isoform) and the kidneys (NHE3 isoform) may serve as a common mechanism that links both disorders and may underlie their interplay. Insulin insensitivity and adipokine abnormalities (the hallmarks of type 2 diabetes mellitus) are characteristic features of heart failure; conversely, neurohormonal systems activated in heart failure (norepinephrine, angiotensin II, aldosterone, and neprilysin) impair insulin sensitivity and contribute to microvascular disease in diabetes mellitus. Each of these neurohormonal derangements may act through increased activity of both NHE1 and NHE3. Drugs used to treat diabetes mellitus may favorably affect the pathophysiological mechanisms of heart failure by inhibiting either or both NHE isoforms, and drugs used to treat heart failure may have beneficial effects on glucose tolerance and the complications of diabetes mellitus by interfering with the actions of NHE1 and NHE3. The efficacy of NHE inhibitors on the risk of cardiovascular events may be enhanced when heart failure and glucose intolerance coexist and may be attenuated when drugs with NHE inhibitory actions are given concomitantly. Therefore, the sodium-hydrogen exchanger may play a central role in the interplay of diabetes mellitus and heart failure, contribute to the physiological and clinical progression of both diseases, and explain certain drug-drug and drug-disease interactions that have been reported in large-scale randomized clinical trials.

Sannino, A., A. Cedars, R. C. Stoler, M. Szerlip, M. J. Mack and P. A. Grayburn (2017). “Comparison of efficacy and safety of transcatheter aortic valve implantation in patients with bicuspid versus tricuspid aortic valves.” Am J Cardiol 120(9): 1601-1606.

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Bicuspid aortic valve (BAV) stenosis has been considered a contraindication to transcatheter aortic valve implantation (TAVI). The aim of this study is to compare the efficacy and safety of TAVI in patients with BAV with those with tricuspid aortic valve (TAV) using balloon-expandable and self-expanding transcatheter heart valves. This retrospective study included 823 consecutive patients with severe, symptomatic aortic valve stenosis undergoing TAVI in 2 institutions, Baylor Heart and Vascular Hospital (Dallas, TX) and The Heart Hospital Baylor Plano (Plano, TX), from January 2012 to February 2016. Efficacy was evaluated by postprocedural valve function as mean gradient, peak velocity, effective orifice area, and >/=moderate paravalvular leak. Safety end points included all-cause 30-day and 1-year mortality, immediate postprocedural mortality and 30-day cardiovascular mortality, procedural success, pacemaker implantation, and procedural complications. Of the 823 included patients, 735 had TAV and 77 had BAV. Baseline characteristics were similar between the 2 groups. Procedural success was high in both BAV and TAV (98.7% vs 99.1%, p = ns). There were no significant differences between groups in valve hemodynamics after TAVI, pacemaker implantation rate, or procedural complications. There were no differences regarding immediate postprocedural mortality (BAV vs TAV, 1.1% vs 0.8%, p = ns), nor 30-day cardiovascular mortality (3.4% vs 2.3%, p = ns). All-cause mortality at 30 days (3.4% vs 3.1%, p = ns) and 1-year (8.5% vs 10.5%) were similar. Patients with BAV showed similar procedural and clinical outcomes to patients with TAV. Therefore, TAVI appears to be a safe and effective procedure for patients with BAVs as well as those with TAVs.

Packer, M. (2017). “Heart failure with a mid-range ejection fraction: A disorder that a psychiatrist would love.” JACC Heart Fail 5(11): 805-807.

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Over the past 5 decades, cardiologists have become obsessed with the ejection fraction. The term can be found in the abstracts of more than 52,000 papers; 10s of 1,000s of additional papers refer to it in their texts. The measurement yields important prognostic information in patients without heart failure, yet the field of heart failure has been particularly consumed by its assessment. We rarely find a paper about heart failure that does not mention it, guidelines mandate its evaluation in all patients, and it has been an entry criterion for every heart failure trial over the past 30 years. Its importance seems odd, however, because ejection fraction is not related to or associated with any specific clinical feature or pathophysiological abnormality of heart failure.