New Era for Ventricular Devices
Surgeons at the Texas Heart Institute in Houston implanted the Jarvik 2000 in a 52-year-old woman with cardiomyopathy, signaling a new era for ventricular assist devices (VADs). The Jarvik 2000 (Figure⇓) is a small, battery-powered axial flow pump that can be used in smaller patients whose bodies are not large enough to accommodate the larger VADs currently approved for use.
O.H. Frazier, MD, codirector of Cullen Cardiovascular Research Laboratories and the chief of cardiopulmonary transplantation at the Texas Heart Institute, implanted the thumb-sized pump in the woman’s chest on April 10 under a protocol approved by the US Food and Drug Administration (FDA). The implant surgery was observed by Stephen Westaby, MD, and his clinical research team from Oxford, UK. The Oxford group initiated a collaborative research project with Drs Jarvik and Frazier in recent years. The FDA has tentatively approved the use of the new small heart-assist device as a bridge to transplant in 5 patients. Dr Frazier said the new pump has many advantages for a variety of patients.
In smaller patients, the pump, which is about the size of a “C” battery, offers a chance to unload the burden on the heart. The miniature intraventricular axial flow pump is only 25 cm3 in volume and weighs 90 g. In this case, Dr Frazier put the Jarvik 2000 in through the left chest rather than the midline, and the patient lost only ≈200 mL of blood, which is much less than the loss seen with the use of the HeartMate or the Novacor device.
The ability to put the pump in through the left chest and the decrease in blood loss makes this device more attractive for use in patients who have had previous heart surgery involving a sternotomy. There is no inlet cannula. A 24-mm disc of apical myocardium is removed with a coring knife. The pump is placed in the apex via a polyester felt reinforced silicone sewing cuff that is sutured to the left ventricular apex, and the outflow graft affixed to the pump is anastomosed to a 16-mm Hemashield graft that is attached to the descending thoracic aorta, said Robert Jarvik, MD, the pump’s developer, who was present for its implantation. The blood is never under great pressure.
The pump’s controller is exterior, with only a 4-mm power cord that leads from the pump and exits from the anterior abdominal wall. Dr Frazier thinks the small size of the power cord makes the threat of infection minor. Initially, the pump was started at 8000 rpm. Once the patient was transferred to the intensive care unit, the pump speed was maintained at 9000 rpm for the first few hours and then increased to 10 000 rpm. Flow remained pulsatile until the speed reached 12 000 rpm. Transthoracic ultrasound showed that the aortic valve opened at 8000 to 9000 rpm but remained closed at 10 000 rpm. Dr Frazier said that once the patient is out of the intensive care unit, the pump will be set to pump 2 liters of blood per minute; the heart must pump the remaining 3 liters of blood. Dr Jarvik noted that, “We maintain pulsatility by only partially unloading the heart.”
The aim is to take the load off the heart, not to replace it, Dr Frazier said. Dr Jarvik observed that chest films taken postoperatively on days 2 and 7 show that cardiomegaly had decreased when compared with preoperative chest films. He also noted that the position of the apex could move as the heart recovers because the apex is not tethered with a cannula crossing the diaphragm. “We believe that mobility of the apex is important to retain optimum ejection dynamics, since the natural motion of the apex toward the aortic valve during systole can be preserved,” he said.
Dr Frazier said the controller can be adjusted by the physician or patient at the bedside or in the office. The patient wears the controller on his or her belt, along with the batteries that provide power.
The pump was used in 1 previous patient under a compassionate waiver from the FDA. However, that patient was very ill and, although the pump operated well for 3 weeks, the patient died of an infection that predated the implant.
Dr Frazier has been collaborating on the development of this VAD with Dr Jarvik. Dr Jarvik first rose to prominence in the mid-1980s when a total artificial heart he developed—the Jarvik-7—was implanted by William DeVries in patients in Utah and Kentucky.
This new VAD is a very different pump. It is an axial flow impeller pump with an outflow graft for anastomosis to the descending thoracic aorta. The pump itself is inserted through a sewing cuff into the apex of the left ventricle. Dr Frazier said hemolysis is not a problem with the pump, which can pump as much as 8 liters per minute.
Dr Jarvik has been working on a continuous flow pump since 1978, and he has been collaborating with researchers at the Texas Heart Institute since 1978. This device has been tested in ≥100 calves.
A major concern was keeping the ceramic bearings lubricated, noted Dr Frazier. Because the bearings are immersed in blood, there is a risk of fibrin and other materials clogging and stopping the bearings and thus the pump. Dr Jarvik would send a version of his pump to the Texas Heart Institute, and researchers would test it and tell him what went wrong. Finally, one version lasted 2 months.
Drs Jarvik and Frazier received private funding for the Jarvik 2000, which allowed them to work on the device until they decided it was right. In 1994, they received a grant from the National Institutes of Health that allowed them to advance the device to clinical trials.
In the future, Dr Westaby, chief of cardiac surgery at Oxford Heart Centre in Great Britain, said he plans to test the pump in his country as a bridge to recovery. Those tests are still unscheduled, but the device has been approved for human trials by the appropriate agency in Britain.
“I want to concentrate on bridge-to-recovery in Oxford,” Dr Westaby said. For that reason, he plans to reroute the power line up through the chest under the skin of the neck to the scalp. The power will go through a titanium pedestal tied to the skull. Dr Westaby thinks this power feed will have a lower risk of infection.
Although Dr Frazier is pleased with the progress of this patient, he would not predict how successful the pump will be in the future. He and Dr Jarvik want to see how well the pump works in the future 4 patients.
With work on VADs taking center stage in the clinical field, the use of the Jarvik 2000 in the United States marks a new chapter in the quest to supplement the abilities of failing hearts.
The Dilemma of Hormone Replacement Therapy
New information from the Women’s Health Initiative adds to the growing debate over whether hormone replacement therapy actually reduces the risk of adverse cardiovascular events. “Prescribing hormone replacement therapy only for cardiovascular benefit may no longer be appropriate,” said Nanette Wenger, MD, professor of medicine (division of cardiology) at the Emory University School of Medicine and director of the cardiac clinics at Grady Memorial Hospital in Atlanta.
On April 4, leaders of the Women’s Health Initiative sent out letters to the women in the hormone replacement therapy portion of the study to tell them that current data from the trial show that during the first 2 years, there was a small increase in the numbers of heart attacks, strokes, and blood clots in the women taking hormones compared with those taking placebo. Over time, the notification continued, the differences between the 2 groups began to get smaller and “may even disappear.” The letter was sent at the recommendation of the Data and Safety Monitoring Board for the trial.
The notification is important because it is the first evidence that hormone replacement therapy may not provide primary prevention for postmenopausal women who have no evidence of heart disease. At the March meeting of the American College of Cardiology, David M. Herrington, MD, MHS, held out hope that hormone replacement therapy might prove valuable in preventing heart disease in apparently healthy women. At that meeting, he reported that the Estrogen Replacement and Atherosclerosis study (ERA) had shown that treatment with estrogen or an estrogen-progesterone combination did not slow the progression of coronary artery disease in women known to have the problem.
“In women with established disease, we have been unable to determine that treatment with these hormones translate into a real benefit,” said Dr Herrington. “That’s not to say that estrogen may not be very effective in those women who do not yet have the disease.” However, the very early trend from the Women’s Health Initiative seems to follow the trend from ERA and the Heart and Estrogen-progestin Replacement Study (HERS) in showing no benefit from hormone replacement therapy.
The ERA study had the following 3 arms: unopposed estrogen replacement, estrogen and progestin replacement, and placebo. Although the end points in the HERS study were non-fatal cardiovascular events and fatal myocardial infarction, the ERA study looked at the progression of coronary disease. Dr Harrington said that an average of 3.2 years of treatment with either estrogen alone or estrogen plus progestin did not slow the progression of the disease in coronary arteries. “These results are indeed somewhat surprising in view of the large body of evidence that estrogen does have good effects on cholesterol and other heart disease risk factors,” he said.
“The single most important message for women with heart disease is to make full use of those forms of therapy that have been shown to slow progression of disease in arteries and reduce risk factors—most notably, reduction of cholesterol,” said Dr Herrington. He, along with others in the field, noted that prescribing hormone replacement therapy can be beneficial for other diseases, such as osteoporosis, possibly Alzheimer’s, and the amelioration of the symptoms of menopause.
The decision to release information from the Women’s Health Initiative could be questioned because the data are not statistically significant. However, trial officials thought they had to notify the women because they had promised to keep the participants notified of all trends in the field. “The fact that it was not statistically significant means you cannot say there is an increase in risk,” said Dr Wenger.
However, the data add weight to other studies that have questioned the cardioprotective effect of hormone replacement therapy. Dr Wenger herself was an investigator in HERS, a national study designed to determine whether hormone replacement therapy can prevent recurrent heart attacks in women who have diagnosed coronary disease after menopause. The HERS study also showed an early rise in the risk of cardiac events with potential late benefit, she said. This trial “was the first to cast doubt.”
However, Dr Wenger is not comfortable saying there is no cardioprotective effect because the data are still not complete. “This is a work in progress,” she noted. She encourages women at her site to stay in the study, as have other investigators at other states around the nation. “There may be a potential for benefit, but we won’t know unless they stay.”
The Women’s Health Initiative involves 40 clinical centers nationwide and has 67 000 women enrolled in its clinical trial portion and 100 000 in an observational study. It was designed to answer these kinds of questions for women.
Dr Wenger said that prior observational studies had led the clinical community to recommend hormone replacement therapy to prevent heart disease. However, those observational studies had significant biases. The real story could only be told with stringent scientific evidence. However, the recommendation became common wisdom.
The new findings, however, cast doubt on that. “Just because ‘everybody knows it’ does not mean that it is correct,” said Dr Wenger.
Link Between Apnea and Hypertension?
Sleep-related disorders and sleep apnea seem associated with hypertension, according to a study funded by the National Heart, Lung, and Blood Institute (JAMA. 2000;283:1829–1836).
Researchers examined the sleep indices of 6132 people who were participating in an ongoing population-based study. Measures of incidences of apnea, hypopnea, percentage of sleep time below 90% oxygen saturation, history of snoring, and the presence of hypertension were made in all the participants.
They found that mean systolic and diastolic blood pressures and the prevalence of hypertension increased with increasing measures that indicated sleep-disordered breathing. The researchers said that some of the association could be explained by body mass index, but even after adjusting for this, smoking, and alcohol consumption, the association remained. The association existed for middle-aged and older participants, with no exclusions for sex, ethnic group, or weight.
In a released statement, Claude Lenfant, MD, the director of the Heart, Lung, and Blood Institute, said, “This is the first study large enough to examine the relationship between sleep apnea and hypertension, independent of other cardiovascular risk factors. It is extremely important since hypertension is a major risk factor for cardiovascular disease… Although these results must be verified, they offer hope that we may be able to reduce cardiovascular mortality in hypertensives by more aggressively diagnosing the apnea.”
- Copyright © 2000 by American Heart Association