Skip to main content
main-content
Top

01-08-2016 | Heart failure | News | Article

Obesity underlies many current-era high-output HF cases

medwireNews: The causes of high-output heart failure (HF) have changed over time, say Mayo Clinic researchers.

The team did not find any instances of thiamine deficiency or Paget’s disease among 120 patients seen at the clinic between 2000 and 2014, and there was only one case of thyrotoxicosis, which was excluded from the analysis on account of being reversible, as were nine cases of severe anaemia.

Instead, obesity accounted for 31% of cases, liver disease for 23% and arteriovenous shunts for 22%. Lung disease accounted for a further 16% and myeloproliferative disorders for 8%.

Relative to 24 controls of similar age and gender to the patients, the HF patients had hyperdynamic hearts, with eccentric right ventricular remodelling and higher ventricular filling and systolic pressures and a markedly higher cardiac output, at 9.5 versus 5.2 L/min.

Notably, Barry Borlaug (Mayo Clinic, Rochester, Minnesota, USA) and study co-authors found that increased metabolic demand contributed to the high cardiac output. Resting oxygen consumption was significantly increased in the patients versus controls, and this was not accounted for by differences in body mass index, with the per kg oxygen consumption being 3.65 versus 2.60 mL/min.

“Increases in flow due to physiological causes, such as exercise or fever, are considered to be normal, but we show that pathological conditions, such as obesity and myelofibrosis, may be associated with increased metabolic demand for tissue perfusion,” they write in the Journal of the American College of Cardiology.

Cardiac output remained increased in the HF patients after accounting for oxygen consumption, however, indicating that it was not the sole cause. But systemic vascular resistance index (SVRI) was significantly reduced in the HF patients versus controls, at 1336 versus 2782 dyne/m2 per s/cm5, and adjusting for this abolished the difference in cardiac output between the two groups.

This suggests “that excessive vasodilation was the stronger pathophysiologic contributor to the high-output state”, says the team.

And vasodilation also contributed to mortality risk. The 3-year mortality rate was 38% in the HF patients (0% in controls), but the rate was 61% among those in the bottom SVRI quartile (<1030 dyne/m2 per s/cm5), compared with 36% among those with normal or only slightly reduced vascular resistance.

Five-year mortality was highest in patients with liver disease and arteriovenous shunts and lowest in those with obesity, at 59% and 58% versus 19%, respectively.

Editorialist Inder Anand (University of Minnesota, Minneapolis, USA) says that physicians should be alert to the possibility of obese patients having high-output HF “that may be erroneously diagnosed as HF with preserved EF (HFpEF)”.

He notes that distinguishing these subtypes can be difficult, and advises clinicians to look out for reduced left ventricular relaxation in patients with HFpEF, with the caveat that this may be simply an effect of age in the elderly.

Some cases may therefore “may need exercise testing with or without invasive evaluation to clarify the pathophysiology”, Anand concludes.

By Eleanor McDermid

medwireNews is an independent medical news service provided by Springer Healthcare Limited. © Springer Healthcare Ltd; 2016

Related topics