Recent studies have shown that vascular calcifications in the pulmonary arteries may contribute to the development of pulmonary arterial hypertension (PAH) through the expression of Runt‐related transcription factor 2, which activates hypoxia‐inducible factor‐1α. This leads to unusual proliferation of pulmonary artery smooth muscle cells and subsequent transdifferentiation into osteoblast‐like cells, promoting further calcification.1 Although pulmonary artery calcifications are rarely seen at the macroscopic in vivo imaging level, similar Runt‐related transcription factor 2–related mechanisms also contribute to calcification of other vascular beds, including the coronary arteries.2 Additional mechanisms, such as loss‐of‐function mutations in bone morphogenetic protein receptor II, also contribute to the development of PAH and vascular calcification.3 We therefore evaluated the relationship between incidentally detected pulmonary arterial dilatation, a noninvasive surrogate for PAH, and the presence of coronary calcifications in patients with normal myocardial perfusion on technetium‐99m sestamibi single‐photon emission computed tomography/computed tomography (SPECT/CT) who also underwent coronary calcium scoring computed tomography.
We performed a retrospective review of 200 consecutive patients from February 1, 2016, to November 30, 2016, who underwent a myocardial perfusion SPECT/CT study with normal myocardial perfusion. The gated computed tomographic images acquired for calcium scoring were reviewed by a nuclear medicine physician, and the mean main pulmonary artery diameter (mPAD) measurement method (as described by Mohammedi and colleagues4) was used to measure mPAD. This method previously showed that mPAD ≥29.5 mm significantly predicted PAH, with a reported sensitivity of 70.8% and specificity of 79.4%.4 Data were gathered for the following variables: age, body mass index, presence of coronary artery calcifications (ie, calcium score >0 was considered significant), medical history of hypertension, renal disease, any past or current smoking, presence of hyperlipidemia, and diabetes mellitus. Except age, all other variables were considered as nominal. We used the chi‐square test to calculate the odds of coronary calcifications in the presence of a dilated pulmonary artery (diameter ≥29.5 mm).
The mean (±SD) age of patients was 58.7 (±10.4) years. The mean mPAD measurement was 26.3 mm (±0.5). In our cohort of 200 consecutive patients with normal myocardial perfusion, 23% (46/200) had mPAD ≥29.5 mm and 33 of 46 (71.7%) persons with mPAD ≥29.5 mm also had coronary calcifications, compared with 80 of 154 (51.9%) persons with mPAD <29.5 mm) (P<.02). The relative risk of persons with mPAD ≥29.5 mm was 1.7 compared with persons with mPAD <29.5 mm who also had coronary calcifications (95% CI, 1.04–2.77). Among persons without hypertension (systolic blood pressure <140 mm Hg) (n=72), there was no difference in the proportion of persons with mPAD ≥29.5 mm who had coronary calcifications (P=.5). However, among patients with hypertension (systolic blood pressure ≥140 mm Hg), the proportion of patients with mPAD ≥29.5 mm who had coronary calcifications was significantly higher (75% vs 55.4%, P=.05). Persons without a history of smoking, hyperlipidemia, or renal disease were 0.45, 0.44, and 0.15 times less likely to have coronary calcifications according to multiple regression analysis, respectively.
Persons with hypertension and increased mPAD have significantly higher odds of having coronary calcifications even with normal myocardial SPECT/CT findings. Differences in end‐diastolic pressures and left ventricular function may contribute to the differences in mPAD.
The lower sensitivity and specificity of mPAD in detecting PAH compared with right‐sided heart catheterization, as shown by Mohammedi and colleagues, might affect these results.4 Further studies incorporating right‐sided heart catheterization with right‐sided heart pressure measurements may be warranted to better investigate the relationship between PAH and coronary calcifications in patients with hypertension.
CONFLICT OF INTEREST STATEMENT
The authors report no conflicts of interest and have no disclosures to declare.
REFERENCES
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