The “placebo effect” may actually work, according to a study published in the September issue of the American Heart Journal. German researchers who verbally signaled to cardiology patients that they would receive a drug (actually a placebo) to improve symptoms saw improvements in coronary blood flow and vasoconstriction, which made chest pain perception decrease.
“Patients with coronary artery disease often show significant clinical improvements in the placebo groups of randomized controlled trials,” Joram Ronel, MD, of the Technische Universität München in Munich, and colleagues wrote. “The extent to which these improvements are due to psychological effects (“placebo effect”) or can be explained by placebo unrelated factors, such as a regression to the mean or spontaneous improvement, remains unclear.”
While decreases of chest pain perception under placebo conditions have previously been observed, Ronel et al set out to evaluate whether placebo-induced chest pain improvement could be the result of changes in coronary blood flow. To do so, Ronel and colleagues enrolled 30 chest pain patients with normal diagnostic angiograms who were assigned to either the verbal signal (VS) group (15 patients) or a control group (15 patients).
The researchers used changes in the percentage diameter stenosis of the coronary arteries as the study’s primary endpoint.
During the study, patients in the VS group received a standardized verbal signal, implying coronary vasodilation. Patients in the control group did not receive a verbal signal. The researchers also reported changes in hemodynamics, psychological distress and chest pain perception.
Ronel and colleagues reported that verbal signals led to vasoconstriction compared with those in the control group. Changes to mean percentage diameter stenosis were 3.2 percent vs. 1.7 percent, respectively. Changes to mean minimal lumen diameter were 0.18 mm vs. 0.06 mm, respectively.
The researchers also reported that chest pain perception was reduced in the VS group compared with the control group. Changes in acute psychological distress did not differ between the two groups, the authors reported.
“In terms of changes in the coronary vessel caliber as adjudicated by quantitative coronary angiography, MLD [minimum lumen diameter] decreased significantly, and percentage DS [diameter stenosis] showed a clear trend toward reduction,” the authors wrote.
“Another important finding is the lack of change in hemodynamic parameters during VS, which argues for the specificity of the effect, rather than for the possibility of a systemic stress reaction leading to a constriction of coronary arteries.”
The authors speculated that the decrease in chest pain perception within the VS group may conclude that this chest pain was not of a coronary origin. “The analgesic placebo effect occurred, even though chest pain perception reduction was not explicitly targeted by the VS,” the authors wrote. Ronel et al noted that this placebo effect could have been due to the fact that patients were under the impression coronary drugs can decrease angina symptoms.
“Our results strengthen the view that coronary physiology can directly be influenced by psychosocial impacts, such as VS and expectations. This enforces a paradigmatic broadening in the understanding of coronary regulation,” the authors concluded. “Regarding high utilization of the health system by chest pain or atherosclerotic patients, our findings might be clinically relevant and help to better comprehend the mechanisms of the brain-heart axis.”