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Daniel L. Dries, MD, MPH, says his team’s study on the racial differences in CHF outcome has generated some concern among the people he is treating.
The report, produced by the Clinical Trials Scientific Research Group at the National Heart, Lung, and Blood Institute in Bethesda, MD, concluded black patients may have a higher risk of heart failure and death from all causes, compared to whites treated in a similar way.
"I’ve had a lot of patients come in to ask about it," Dries says, a cardiology and clinical trials research fellow. But he doesn’t let the news intimidate them. Instead, he explains how scientists are piecing together evidence suggesting a black patient faces the most severe outcomes if CHF runs out of control — and the body’s response to a failing heart may be even more dramatic than in other groups of patients. That means it’s time to really get to work on controlling the disease.
"Rather than get discouraged, my patients get very motivated to be seen in the clinic, to take medication, and to exercise."
Dries and the other researchers from his team didn’t have to start their study from scratch. They used the prevention and treatment phases of the 1990 Studies of Left Ventricular Dysfunction (the SOLVD trial) as a starting point. Patients had already been assembled and randomized to either enalapril or a placebo, and the data were already there to analyze according to the racial background of the patients and their results.
"It gave us a great opportunity to sort out if there was independent association with race and bad outcomes," Dries says.
At the beginning of both the prevention and treatment trials of the SOLVD study, these characteristics were different between black and white participants:
Blacks and whites had similar average systolic blood pressure and equal randomization to either enalapril or placebo.
In both trials, more black patients died of pump failure, stroke, and pulmonary embolism. (Dries’s group included in the pump failure end point what the SOLVD study termed "probable arrhythmia with some antecedent worsening of heart failure.")
Dries’s group combined the prevention and treatment trials and statistically adjusted for the primary variables of the study, as well as socioeconomic issues such as the financial distress and amount of education.
Blacks had a higher relative risk of dying from all causes, pump failure, and a combined end point for death from any cause or hospitalization for heart failure. When the team adjusted the variables according to the separate trials, blacks still had a higher relative risk of dying from all causes. (Although the relative risk was reduced from the prevention trial to the treatment group: 1.46 and 1.22 respectively.)
"I was a little bit surprised," Dries says. "I thought after we readjusted for these risks, they would disappear. But even after we readjusted, the differences were still there."
What could have caused the differences in outcomes between whites and blacks? The team reported it probably wasn’t a difference in ACE inhibitor sensitivity, since blacks were randomized to both a placebo and enalapril.
Dries notes there were some indications blacks had higher levels of catecholamines, which could indicate the neurohormonal response to heart failure may be different according to the race of the patient.
The hypothesis is difficult to prove with this data set because the numbers of black patients in some of the trials were too small to be conclusive. It’s easy to see that black patients developed heart failure at a younger age, however, and developed more fibrosis. And on an anecdotal level, Dries says the study should bring nods of agreement from cardiac specialists.
"I think if you talk to most cardiologists and ask them if black patients tend to do worse, the answer would be yes.’"
One cardiologist may have another explanation, however. Charles Curry, MD, chief of cardiovascular disease at Howard University in Washington, DC, says it’s important to consider how long it may take black and white patients to develop heart failure. An African-American who develops heart failure after first becoming hypertensive at a young age may have a longer buildup than a white patient, although both may be in the same functional stage when they are compared in a study.
"The result is a longer time to cause destruction to the heart muscle," Curry says.
"I thought we did a good job in adjusting for risk," Dries responds, but notes it could explain some of the findings. Dries adds he wishes the SOLVD study included the amount of time it took individual patients to develop the disease. Studies going on now such as the BEST trial will be looking at the development of neurohormones over time.
"They’ll be able to test the hypothesis that we proposed," he says, adding that even before doctors figure out the biochemical nuances between the races, the third-generation beta-blockers may be especially useful to treat black patients.