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A HIGH resting heart rate is increasingly being recognised as a marker for increased mortality, according to a leading Australian cardiologist.
A new meta-analysis, published last week in the Canadian Medical Association Journal, found that the risk of all-cause and cardiovascular mortality increased by 9% and 8% respectively for every 10 beats/minute increment of resting heart rate. Compared with 45 beats/min, the all-cause mortality risk increased significantly with increasing resting heart rate in a linear relation, with a significantly increased risk of cardiovascular mortality observed at 90 beats/min. (1)
Professor Garry Jennings, director of the Baker IDI Heart and Diabetes Institute, told MJA InSight that resting heart rate was “certainly coming through as a marker of increased mortality risk”.
However, Professor Jennings cautioned that heart rate was not as strong as traditional risk factors such as having had a previous heart attack or stroke, and that it remained unclear whether it was intrinsically harmful, or a marker of underlying disease.
The latest meta-analysis was based on 46 studies involving 1 246 203 patients and 78 349 deaths for all-cause mortality, and 848 320 patients and 25 800 deaths for cardiovascular mortality.
The relative risk with 10 beats/min increment of resting heart rate was 1.09 for all-cause mortality and 1.08 for cardiovascular mortality. Patients with a resting heart rate of 60–80 beats/min had a relative risk of 1.12 for all-cause mortality and 1.08 for cardiovascular mortality, but those with a resting heart rate greater than 80 beats/min had a relative risk of 1.45 for all-cause mortality and 1.33 for cardiovascular mortality.
The researchers wrote that a resting heart rate of 90 beats/min was consistent with the traditionally defined tachycardia threshold.
“Overall, the results did not differ after adjustment for traditional risk factors for cardiovascular disease”, they wrote.
The results warranted further research to develop a prediction algorithm that would consider both resting heart rate and classic cardiovascular risk factors so physicians could use resting heart rate in clinical settings, they wrote.
Professor Jennings said there were “a number of relatively common medical conditions associated with increasing heart rate, including neuropathy in diabetes, heart failure [and] overactive thyroid and it is impossible to adjust for all of these in the studies”.
Although tachycardia could be treated directly with drugs such as beta-blockers or ivabradine, this was not recommended unless the patient complained of symptoms, he said.
The CMAJ meta-analysis included a 2006 study in geriatric patients led by Associate Professor Alex Fisher, a specialist in geriatric medicine based at the Australian National University and Canberra Hospital.
Dr Fisher told MJA InSight that caution was needed when translating the research findings into the geriatric setting.
“In a younger person 45 beats per minute is okay, but in the elderly, less than 60 beats per minute can be as dangerous as over 90 beats per minute”, he said.
Tachycardia should be taken seriously in elderly patients given its association with mortality, but taking into account “the full picture, not just this one symptom”, Dr Fisher said.
“Tachycardia may be related to undiagnosed comorbidities, or to medication the patient is on such as anticholinergics, or to psychological stress and so on”, he said.
The authors of the meta-analysis admitted that a concern from their results was whether a high resting heart rate was an independent predictor, because higher heart rates coexist with traditional risk factors of cardiovascular disease and poor health status.
However, they wrote that overall their findings showed that the association of resting heart rate with risk of all-cause and cardiovascular mortality “is independent of traditional risk factors of cardiovascular disease, suggesting that resting heart rate is a predictor of mortality in the general population”.
(Photo: Amawasri Pakdara / shutterstock)
Like Troponins, some physiological “predictors” of poor outcomes are almost self-defining. We know, for example, that the elderly with diffuse coronary disease will leak Troponin when they have poor systemic perfusion – such as in septic shock. We now know that the raised Troponin correlates with poor outcome, but we already knew this about septic shock in the elderly anyway. I’m not sure we are gaining much my looking for correlations between test-based measures and outcomes when we already know that frailty is a risk factor in itself. Maybe it’s too easy to publish the results of data dredges.
clearly this is likely to be confounding