Comparison of ultrasound-measured properties of the common carotid artery to tobacco smoke exposure in a cohort of Indonesian patients

Background: With 72% of Indonesia males over 15 years old who smoke, Indonesia has one of the highest incidences of tobacco use in the world. Smoking is the most significant lifestyle factor that contributes to development of... [ view full abstract ]

Background:
With 72% of Indonesia males over 15 years old who smoke, Indonesia has one of the highest incidences of tobacco use in the world. Smoking is the most significant lifestyle factor that contributes to development of stroke, the leading cause of death in Indonesia. The effects of smoking include alteration of arterial stiffness and carotid intima-media thickness (CIMT), measures that reflect vascular health and stroke risk. Exposure to secondhand smoke (SHS) can also induce unfavorable vascular changes in individuals. We attempted to use ultrasound to relate exposure to tobacco smoke, either primary or secondary, with CIMT and measures of common carotid artery (CCA) stiffness. We also aimed to determine whether first-year medical students could be trained to accurately measure these vascular properties in patients.

Methods:
Patients and employees of multiple clinics associated with Dinas Kesehatan, the public health department of the city of Bandung, West Java, Indonesia, were recruited for the study. Demographic information and health history were obtained via questionnaire. Blood pressure and resting heart rate were measured before and after the scan. Patients were scanned using the NanoMaxx® ultrasound system (Sonosite, Bothell, Washington, USA) attached to a linear 7.5 mHz probe. CIMT was measured using the NanoMaxx's software with the CCA visualized longitudinally in B-mode. The NanoMaxx was then switched into M-mode and 5 rounds of systole and diastole captured. End-systolic and end-diastolic CCA diameter was measured for each round and averaged.

The following equations were used to calculate indices of arterial stiffness:
Distensibility coefficient: DC=2×∆d/(∆p×d_s)
Cross-sectional compliance: CC=(∆d/d_s)/(2×∆p)×π×d_s^2
β-Stiffness: β = [ln(SBP/DBP)×d_d]/∆d
Young’s elastic modulus: YEM=K×d_d×∆p/∆d

Where:
SBP = average systolic blood pressure
DBP = average diastolic blood pressure
d_d = average diastolic CCA diameter
d_s = average systolic CCA diameter
Δd = d_s - d_d
Δp = SBP - DBP
K = a constant equalling 133.3

Multiple regression was performed to compare tobacco smoke exposure and other cardiovacular risk factors to to CIMT and values of arterial stiffness. Simple linear regression was performed to correlate CIMT with each measure of stiffness described above. A two-sided t-test was performed to compare CIMT and stiffness of patients with history of myocardial infarction (MI) and/or stroke versus patients with no history.

Results:
Tobacco smoke exposure exhibited a weakly negative correlation with indices of stiffness and a weakly positive correlation with CIMT in individuals who smoked. Age seemed to contribute the most for the variation between individuals. Exposure to SHS exhibited a weakly positive correlation with both stiffness indices and CIMT. Age and BMI contributed the most for the variation between individuals. In the smoking group, there was a weakly positive correlation between CIMT and distensibility. In the SHS group, there were weakly positive correlations between CIMT and stiffness, as well as CIMT and YEM. Patients with history of acute cardiovascular event had significantly decreased DC relative to patients without history of cardiovascular event. Patients with history of MI/CVA also trended towards having a higher CIMT than individuals without such history, but the comparison did not reach statistical significance.

Discussion:
The weak effect of tobacco smoke exposure on our measured CCA properties was unexpected. Associations between smoking and increased CIMT are well-documented in the literature. Previous attempts to compare smoking and stiffness have not shown strong correlations. Other studies have also found that smoking is actually associated with decreased arterial stiffness, which may explain why smoking is the largest modifiable risk factor for development of abdominal aortic aneurysm (AAA). We did successfully show that individuals with previous stroke or MI exhibited increased carotid stiffness and CIMT, though a larger sample size may have increased the statistical significance of our comparison further.

One possible reason for the decreased correlation coefficient may have been our limited ability to assess cardiovascular risk. We were also unable to account for white coat hypertension, especially since many participants do not encounter foreigners regularly. Anatomic variation also made accurate CIMT and M-mode measurements difficult at times. We also could not account for possible differences in pollution exposure, which may also play a role in physical properties of the CCA. In conclusion, we demonstrated that medical students could successfully perform various ultrasound measurements of the CCA and match previous findings in the literature.