Cardiovascular disease, like hypertension, is one of the top killers of human life and early detection of cardiovascular disease is of great importance. However, traditional medical devices are often bulky and expensive, and unsuitable for home healthcare. In this paper, we proposed an easy and inexpensive technique to estimate continuous blood pressure from the heart sound signals acquired by the microphone of a smartphone. A cold-pressor experiment was performed in 32 healthy subjects, with a smartphone to acquire heart sound signals and with a commercial device to measure continuous blood pressure. The Fourier spectrum of the second heart sound and the blood pressure were regressed using a support vector machine, and the accuracy of the regression was evaluated using 10-fold cross-validation. Statistical analysis showed that the mean correlation coefficients between the predicted values from the regression model and the measured values from the commercial device were 0.707, 0.712, and 0.748 for systolic, diastolic, and mean blood pressure, respectively, and that the mean errors were less than 5 mmHg, with standard deviations less than 8 mmHg. These results suggest that this technique is of potential use for cuffless and continuous blood pressure monitoring and it has promising application in home healthcare services.
Heart rate variability is a useful clinical tool for autonomic function assessment and cardiovascular disease diagnosis. To investigate the dynamic changes of sympathetic and parasympathetic activities during the cold pressor test, we used a time-varying autoregressive model for the time-frequency analysis of heart rate variability in 101 healthy subjects. We found that there were two sympathetic peaks (or two parasympathetic valleys) when the abrupt changes of temperature (ACT) occurred at the beginning and the end of the cold stimulus and that the sympathetic and parasympathetic activities returned to normal in about the last 2 min of the cold stimulus. These findings suggested that the ACT rather than the low temperature was the major cause of the sympathetic excitation and parasympathetic withdrawal. We also found that the onsets of the sympathetic peaks were 4-26 s prior to the ACT and the returns to normal were 54-57 s after the ACT, which could be interpreted as the feedforward and adaptation of the autonomic regulation process in the human body, respectively. These results might be helpful for understanding the regulatory mechanisms of the autonomic system and its effects on the cardiovascular system.
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