Contemporary Medical Options for Treating Patients With Heart Failure

Abstract

ase study: A 72-year-old woman presented with shortness of breath. Three months earlier, she had begun to notice dyspnea on exertion. This dyspnea progressed to the point that she noted dyspnea at rest in the 24 hours before presentation. She had a history of long-standing mild hypertension, treated with a calcium-channel antagonist, and type 2 diabetes. She denied chest pain, lightheadedness, and abdominal or ankle swelling, although she believed that she had gained between 5 and 10 pounds in recent weeks. On examination, she had a blood pressure of 150/90 mm Hg, a regular pulse at a rate of 90 min Ϫ1 , jugular venous pressure of about 8 cm water, faint bibasilar crackles, a prominent and displaced apical impulse, and a summation gallop, with no murmurs, no organomegaly, or ascites, but with 1ϩ ankle edema. Laboratory findings were notable for a creatinine level of 2.0 mg/dL, a random blood sugar level of 220 mg/dL, and proteinuria (protein:creatinineϭ400 mg/g). Her ECG showed sinus rhythm, left atrial enlargement, left ventricular hypertrophy (LVH), Q waves in the inferior leads, and inferolateral ST-and T-wave changes. The ECG findings were unchanged, except for a heart rate that had increased from a tracing taken 6 months earlier. Her chest x-ray showed a mildly enlarged cardiac silhouette and questionable evidence of pulmonary venous congestion. An echocardiogram showed a moderately dilated left ventricle with increased wall thickness, inferobasilar akinesis, and an ejection fraction estimated between 30% and 35%.

Is Depressed Myocyte Contractility Centrally Involved in Heart Failure?

“…1,3 It is also well appreciated that treating heart failure patients with drugs (such as cardiac glycosides) that augment pump function by increasing the contractility of cardiac myocytes can improve hemodynamics and exercise tolerance. 4 These early observations led to the "hemodynamic hypothesis" that heart failure is primarily caused by defective cardiac myocyte contractility. The purpose of this review is to identify and discuss unanswered questions (listed below) related to this hypothesis.…”

Evidence‐based drug treatment of chronic heart failure

“…ACE inhibitors are indicated in all stages of left ventricular dysfunction irrespective of symptoms. 2 These drugs should be started as early as possible after identification of the condition and after adequate diuresis. Once initiated, the ACE inhibitor dose should be increased steadily to the maximal tolerated or target dose.…”

“…2 However, manipulation of concomitant therapy may be all that is required, in particular potassium-sparing diuretics and other agents with an effect on renal function, eg NSAIDs, may need to be discontinued. Thereafter, referral for investigation and consideration of renal artery stenosis may be warranted.…”

Thoracic organ transplantation

“…It is also possible, however, that transplant teams removed candidates from the active list when death was imminent, artificially reducing program-specific and overall waiting list mortality. Although the total number of candidates initially listed as Status 1A has steadily increased from 1999 to the end of 2002, the death rate for this critically ill group has also declined dramatically, from 1399 per 1000 years at risk in In summary, despite great advances in the detection, prevention, and management of heart failure, there continue to be more candidates for heart transplant than there are available donor organs deemed suitable for use (6)(7)(8). After being placed on the waiting list, patients face one of three competing outcomes: transplantation, death on the waiting list, or removal from the waiting list.…”