The study, which measured the chronic consumption of caffeinated products over a 12-month period, rather than acute consumption, appears in the Journal of the American Heart Association. It is the largest to date to have evaluated dietary patterns in relation to extra heartbeats.

“Clinical recommendations advising against the regular consumption of caffeinated products to prevent disturbances of the heart’s cardiac rhythm should be reconsidered, as we may unnecessarily be discouraging consumption of items like chocolate, coffee and tea that might actually have cardiovascular benefits,” said senior author Gregory Marcus, MD, MAS, a UCSF Health cardiologist and director of clinical research in the UCSF Division of Cardiology.

Excessive premature atrial contractions (PACs) have been shown to result in atrial fibrillation, stroke and death, while excessive premature ventricular contractions (PVCs) have been shown to result in increased heart failure, coronary artery disease and death. Both abnormalities have been tied to caffeine consumption through studies and trials, but these studies were performed several decades ago and did not use PACs and PVCs as a primary outcome.

Nonetheless, the American College of Cardiology/American Heart Association guidelines on the management of PVCs state that if a patient’s history is consistent with premature extra beats, potential exacerbating factors such as caffeine, alcohol and nicotine should be eliminated. Other online medical resources for clinicians offer similar recommendations.

Recent growing evidence indicates the potential cardiovascular benefits of several common caffeinated products such as coffee, chocolate and tea. The result is clinician uncertainty in counseling patients on consumption of these products, with patients possibly reducing their intake to avoid presumed cardiac issues.

In their study, Marcus and his colleagues analyzed 1,388 randomly selected participants from the National Heart, Lung and Blood Institute (NHLBI) Cardiovascular Health Study database of nearly 6,000 patients, excluding those with persistent extra heartbeats. They were given a baseline food frequency assessment and 24-hour ambulatory electrocardiography monitoring. Frequencies of habitual coffee, tea and chocolate consumption were determined through a survey.

Of the total participants, 840 (61 percent) consumed more than one caffeinated product daily.

The researchers found no differences in the number of PACs or PVCs per hour across levels of coffee, tea and chocolate consumption. More frequent consumption of these products was not associated with extra heartbeats.

“This was the first community-based sample to look at the impact of caffeine on extra heartbeats, as previous studies looked at people with known arrhythmias,” said lead author Shalini Dixit, BA, a fourth-year medical student at UCSF. “Whether acute consumption of these caffeinated products affects extra heartbeats requires further study.”

“Aging affects everyone and causes changes throughout our bodies,” said Erika Boerman, PhD, a post-doctoral fellow in the Department of Medical Pharmacology and Physiology at the University of Missouri School of Medicine and lead author of the study. “The purpose of our study was to understand how blood vessels are affected by this process. We found that older arteries had a significantly lower number of sensory nerves in the tissues surrounding them and they were less sensitive to an important neurotransmitter responsible for dilation.”

Boerman’s study focused on mesenteric arteries ― a type of artery that supplies blood to the small intestines ― of mice that were 4 months and 24 months old. These ages correspond to humans in their early 20s and mid-60s, respectively. Without stimulation, the diameter of the blood vessels of both younger and older mice was approximately the same. However, when stimulated to induce dilation, differences between the age groups became apparent.

“The younger arteries dilated as expected,” Boerman said. “However, when we performed the same stimulation to the arteries of older mice, the vessels did not dilate. When we examined the presence of sensory nerves, we noted a 30 percent decrease in the amount surrounding the older arteries compared to the younger arteries.”

According to a news release from the medical school, the researchers found that even when purposefully exposing older mesenteric arteries to defined amounts of the neurotransmitter calcitonin gene-related peptide, or CGRP, the arteries’ ability to dilate was greatly reduced.

“Poor neurotransmitter function and a reduced presence of sensory nerves surrounding older vessels lead to age-related dysfunction of mesenteric arteries,” Boerman said. “The importance of this discovery is that if we can identify why this happens to mesenteric arteries, it may be possible to prevent the same thing from happening to other blood vessels throughout the body.”

More research is needed to understand why aging affects sensory nerve distribution and neurotransmitter performance. However, identifying this new mechanism of vascular dysfunction opens the door for future studies that could eventually lead to the treatment of health issues such as stroke and cardiovascular disease.

The findings were published in the Journal of Physiology.