SPRINT results reinforce connection between hypertension, HF
BOSTON — In the SPRINT trial, intensive BP therapy conferred reduced risk for CV events largely through reduction in HF, confirming research that has established hypertension as a major contributor to HF, an expert said at Cardiometabolic Health Congress.
Several trials since the late 1990s have shown that “there is a consistent signal that the treatment of hypertension does lead to reduction in the incidence of HF,” Clyde W. Yancy, MD, MSc, professor of medicine and medical social science, chief of cardiology, associate director of the Bluhm CV Institute and vice dean of diversity and inclusion at Northwestern University Feinberg School of Medicine, said.
In the SPRINT population, reduction in mortality also was driven by reduction in HF. “I get excited thinking about this, to do something fundamental for the prevention of HF,” Yancy, past president of the American Heart Association and deputy editor of JAMA Cardiology, said. “A mediocre physician treats disease; a great physician prevents disease.”
The importance of HF prevention was underscored by a 2007 study (Ammar KA, et al. Circulation. 2007;doi:10.1161/CIRCULATIONAHA.106.666818) finding that patients with the precursor stages A and B of HF had an almost 100% survival rate 8 years after diagnosis, but patients with stage C HF were far less likely to survive to 8 years, and patients with stage D HF did not survive past 6 years (log-rank P < .0001), he said.
Analyses of several large cohorts have indicated that hypertension, diabetes and obesity were associated with onset of HF, and people with at least one of those conditions tend to die 3 to 11 years earlier than those without any, Yancy said.
Other research has shed light on how hypertension might lead to HF, he said, noting that one well-known path is that hypertension leads to increased risk for MI, and individuals with myocardial injury are more likely to develop HF.
It has also been suspected that cardiomyopathy might be a connection between the two conditions, and recent literature has uncovered some possible mechanisms, according to Yancy.
“Victor Dzau, MD, has suggested that perhaps this progression comes uniquely from the intersection of neurohormonal activation, angiotensin II, hypertension and oxidative stress,” Yancy said. “This oxidative stress story is important because it puts nitric oxide at the center of the equation. We believe that nitric oxide is one of the mechanisms that leads to the vulnerability” of black individuals for HF.
Another theory is that the progression from hypertension to HF is accelerated by excessive consumption of inorganic phosphates. “At Northwestern, we believe that phosphate may become the new sodium because it’s been underrecognized that it participates in deleterious pathways and may in fact lead to hypertrophy,” he said. “When we ingest phosphates, it elicits a signal of fibroblast growth factor 23. When the source of the phosphorous is organic, that works in a well-defined pathway that generates the correct homeostasis in bone calcium. But consumption of inorganic phosphorous may lead to a pathway that generates hypertrophy and other cardiac remodeling. We are testing this prospectively in [an ongoing study] as a way of trying to tease out why certain at-risk communities have a higher burden of HF.”
This research reinforces that “there are potentially important mechanisms that may be modifiable that are taking us from hypertension to HF and allow us to understand who is uniquely at risk for HF,” he said.
What SPRINT and other literature has reinforced, he said, is that controlling hypertension does reduce the incidence of HF. “There is a profound opportunity to reduce the incidence of HF, especially in those at high CVD risk.” – by Erik Swain
Yancy CW. Heart Failure in the Context of SPRINT: What has Changed? Presented at: Cardiometabolic Health Congress; Oct. 5-8, 2016; Boston.
Disclosure: Yancy reports no relevant financial disclosures.