"The failing heart is not just an enlarged version of a normal heart." I know Dr. Louis Katz said it, but I never found out where. At any rate, he posthumously alerted me to recognize that patients with heart failure do not demonstrate the lower range of normal physiology, but rather their own special ranges. I recognize this in the exquisite load sensitivity of the failing heart or in noting how much atrioventricular synchrony contributes to the failing heart. I try to teach this all the time-I'll know it's time to retire when I overhear the medical students joking about me having them graph the relationship between cardiac output and vascular resistance. Nevertheless, it's a concept I use every day.-Marc A. Silver Similar to all disease states, the primary approach to and ultimate treatment of heart failure is prevention. For the entire human population, this means bringing systemic blood pressure into the currently recommended range, controlling the risk factors for atherosclerosis, aggressively managing ischemic syndromes, reversing valvular and congenital lesions before cardiac damage occurs, and so forth. Hopefully, over time, we'll be able to counter and reverse many of the predisposing genetic factors as well.-Carl V. Leier Ask patients to describe exactly how they take their medications. Heart failure patients are frequent victims of polypharmacy, and despite the best intentions of the health care providers and patients, inadvertent medication errors are common. For example, one of my patients mixed up his digoxin and isosorbide dinitrate; as a result, he was taking digoxin three times a day (and wondering why he was nauseated)! Ask routinely about the use of over-the-counter medications, especially cold preparations, "diet pills," and nonsteroidal anti-inflammatory drugs (NSAIDs). These widely available agents are frequently used by heart failure patients, who fail to recognize the potential for drug-drug and drug-disease interactions.-Michael W. RichThere are several things I routinely do for each patient who comes to see me. On the first visit, I examine current medications and simplify the regimen. I eliminate calcium channel blockers, NSAIDs, and albuterol (unless there is a pressing need to continue these). We routinely check digoxin levels and adjust the medication to keep the plasma level between 0.7 and 1.0 ng/mL. This is based on data from our laboratory showing that most of the benefit of this drug is at low dose (J Am Coll Cardiol. 1997;29:1206) and a post hoc analysis of the DIG study, which showed a relationship of plasma level and mortality with more toxicity at higher doses (Am Heart J. 1997;134:3). I optimize angiotensin-converting enzyme (ACE) inhibitor doses (in an attempt to use the doses shown to be efficacious in the clinical trials) and use a longer-acting, preferably once-a-day ACE inhibitor to simplify the patient's regimen. I often give this dose prior to bedtime so that any hypotension will be at night while the patient is sleeping. I also give nitrates to my heart failure pat...

Embolism remains a significant complication of the total artificial heart (TAH). The ineffectual deairing of the TAH can allow embolization of the retained air. The standard needle aspiration of TAH air (Group A) was compared with a new protocol (Group B) that included standard needle TAH aspiration plus simultaneous pumping of the TAH against an occluded ascending aorta and main pulmonary artery with vacuum applied to a needle in the proximal aorta and pulmonary artery. There were 4 calves in each group. There was no premortem evidence of systemic or pulmonary emboli. Both groups of animals were electively terminated less than 2 weeks postoperatively. Postoperative mean aortic and pulmonary artery pressures were recorded for each animal. Animals in Group B had a significant decline in pulmonary artery pressures (43 & 12 vs. 33 & 8 mm Hg) 1 h after TAH implantation when compared with Group A. All other aortic and pulmonary artery pressure differences between Groups A and B were not statistically significant within 24 h of the operation. Group A animals had a 75% incidence, and Group B animals had 100% incidence of TAH thrombus. This very small thrombus was found exclusively at the inflow valve-TAH housing interface. Evaluation of the kidneys postmortem was used to identify embolic injury. All animals in Group A had evidence of acute, hemorrhagic injury, but none of the Group B animals had similar injury. Half of the animals in each group had small, fibrotic chronic renal cortical injury, which did not develop during TAH implantation. The more vigorous deairing protocol (Group B) significantly decreased early postoperative pulmonary hypertension. The absence of acute hemorrhagic renal injuries appeared to be associated with improved TAH deairing. Chronic renal injuries were not associated with the TAH, which makes them poor indicators of TAH emboli. Improved TAH deairing can provide

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