Mechanical Circulatory Support
In the present issue of Circulation, Drs Frazier and Delgado1 and Drs Stevenson and Rose2 emphasize the enormity of the problem congestive heart failure represents. It is now the major cardiovascular problem in the world. They also describe the history of surgical treatments for heart failure, including the development of the left ventricular assist devices (or, as Drs Frazier and Delgado1 refer to them, mechanical circulatory support [MCS] devices) and of cardiac transplantation. Frazier and Delgado1 and Stevenson and Rose2 very thoughtfully describe what they believe the future for MCS may be and point out the importance of identifying patients best suited to receive these devices, as well as the need for further development. Drs Stevenson and Rose2 emphasize the importance of considering patients for MCS who have already been maximally treated medically and have clearly failed such therapy. Drs Frazier and Delgado1 emphasize similar issues, but express their optimism for continued development of MCS and their role in earlier treatment of heart failure to avoid end-organ damage. In evaluating MCS devices that have been developed to date, one cannot help but be impressed by the Jarvik 2000, which has now been used in 12 patients at the Texas Heart Institute/St Luke’s Episcopal Hospital in Houston, Tex, for more than 1 year. One patient was supported successfully for 3 years. In all instances, patients discharged from the hospital returned to a New York Heart Association functional class I status without significant infection associated with the implantation or use of the device. Dr Frazier has placed this device in patients’ hearts without cardiopulmonary bypass, which further reduces risk of bleeding and organ injury. Thus, one looks forward to the further development of this device and others of similar size and capability.
Heart failure is an enormous problem in the United States and the world today. As pointed out above, some 5 million patients currently have heart failure in the United States, and 1 in 5 men and women have a risk of developing heart failure during their lifetime. Medical treatments of heart failure have consistently improved, and today, the administration of selected β-blockers, angiotensin-converting enzyme inhibitors, and aldosterone antagonists reduces the risk of death and improves symptoms of patients with heart failure. Nevertheless, both morbidity and mortality remain high in patients with class III and IV heart failure, and additional therapies need to be identified.
We must identify mechanisms responsible for heart failure. Although we know that excessive alcohol consumption in individual patients and selected viral infections of the heart lead to heart failure in some patients, the precise mechanisms responsible for heart failure and its progression are not well elucidated. We are limited in our ability to interrupt relentless progression of heart failure in patients, irrespective of etiology and even with the advances that have been made in medical therapies. With the continued aging of the population, one expects heart failure to increase in frequency. Thus, there is a critical need to identify specific etiologies responsible for heart failure, mechanisms of cellular and subcellular injury, and therapies that interrupt and/or correct organellar and cellular injury. It should be helpful to find ways to deliver genes and correct protein abnormalities that play a significant role in the development, initiation, and progression of heart failure.
One should also be interested in the early work with stem cell therapies in patients with heart failure. Two German groups, one led by Dr Bodo Strauer and colleagues and the other by Drs Zeiher and Dimmeler, as well as a group at the Texas Heart Institute/St Luke’s Episcopal Hospital and the Hospital Procardico in Rio de Janeiro, Brazil, led by Drs Perin, Dohman, and Willerson, have shown that bone marrow–derived stem cells given directly into the coronary artery in patients with recent infarction (Strauer and Zeiher and Dimmeler’s studies) or to patients with chronic heart failure and severe left ventricular dysfunction after earlier myocardial infarctions (Drs Perin, Dohman, and Willerson) may improve blood flow and function of the heart in relatively small numbers of patients that have been treated and followed for 6 months or longer. This appears to be an area of future promise. Stem cells might serve as a vector for genes in the future that could be used relatively early in patients with heart failure with the generation of new heart muscle cells, improved blood flow, and potential correction of gene/proteomic abnormalities in the failing heart. This form of therapy might ultimately be complementary to MCS, and it might even be possible to use MCS for a relatively short period of time, if stem cells play a major role in regenerating and repairing injured heart muscle.
At the bottom line, however, the primary issue will still relate to which patients should receive MCS or stem cells and when in their clinical courses. We have taken poetic license with the concluding paragraph of Drs Frazier and Delgado’s article.1 Shakespeare’s Hamlet is cited, as Hamlet advised “The Players” by suggesting that one must suit the action in this case to the individual patient’s problem. This is excellent advice to all concerned with the development of improved therapies for patients with heart failure. Nevertheless, this is an exciting area for further clinical research, and one in which effective treatments that prevent the initiation and/or progression of heart failure are badly needed.
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
Frazier OH, Delgado RM. Mechanical circulatory support for advanced heart failure: where does it stand in 2003? Circulation. 2003; 108: 3064–3068.
Stevenson LW, Rose EA. Left ventricular assist devices: bridges to transplantation, recovery, and destination for whom? Circulation. 2003; 108: 3059–3063.