False Heart Rate Feedback and the Perception of Heart Symptoms in Patients with Congenital Heart Disease and Anxiety

Background Little is known about the mechanisms explaining an increased perception of heart symptoms in congenital heart disease (ConHD). In the present study, it was suggested that a combination of high trait anxiety and disease history increases the perception of heart symptoms. Purpose It was tested whether false heart cues will result in an increased perception of heart symptoms in patients with ConHD and anxiety. Method Thirty-six patients with ConHD and 44 healthy controls performed two exercise tasks. During one of the exercise tasks, participants were exposed to a false heart cue consisting of false heart rate feedback (regular or irregular). Perceived heart symptoms were assessed and heart rate, arterial partial pressure of CO2, and respirator rate were monitored continuously. Results In line with the predictions, false heart rate feedback resulted in an increased perception of heart symptoms in high trait anxious patients with ConHD that could not be explained by acute heart dysfunction. However, unexpectedly, this effect was not observed immediately after the false heart rate feedback task but after a second exercise task without false feedback. Conclusion The results suggest that not the sole presence of ConHD but ConHD in combination with high trait anxiety results in a vulnerability to overperceive heart symptom

Cardiac troponins: from myocardial infarction to chronic disease.

Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to-date has been developed: cardiac troponin (cTn) assays. For the past decade, cTn has been regarded as the gold-standard marker for acute myocardial necrosis: the pathological hallmark of acute myocardial infarction (AMI). Whilst cTn is the cornerstone for ruling-out AMI in patients presenting with a suspected acute coronary syndrome (ACS), elevated cTn is frequently observed in those without clinical signs indicative of AMI, often reflecting myocardial injury of 'unknown origin'. cTn is commonly elevated in acute non-ACS conditions, as well as in chronic diseases. It is unclear why these elevations occur; yet they cannot be ignored as cTn levels in chronically unwell patients are directly correlated to prognosis. Paradoxically, improvements in assay sensitivity have meant more differential diagnoses have to be considered due to decreased specificity, since cTn is now more easily detected in these non-ACS conditions. It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasising the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasising a need to understand the mechanisms of such release. This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases