Coronary microvascular function and myocardial fibrosis in women with angina pectoris and no obstructive coronary artery disease: the iPOWER study

Abstract

BackgroundEven in absence of obstructive coronary artery disease women with angina pectoris have a poor prognosis possibly due to coronary microvascular disease. Coronary microvascular disease can be assessed by transthoracic Doppler echocardiography measuring coronary flow velocity reserve (CFVR) and by positron emission tomography measuring myocardial blood flow reserve (MBFR). Diffuse myocardial fibrosis can be assessed by cardiovascular magnetic resonance (CMR) T1 mapping. We hypothesized that coronary microvascular disease is associated with diffuse myocardial fibrosis.MethodsWomen with angina, a clinically indicated coronary angiogram with <50 % stenosis and no diabetes were included. CFVR was measured using dipyridamole (0.84 mg/kg) and MBFR using adenosine (0.84 mg/kg). Focal fibrosis was assessed by 1.5 T CMR late gadolinium enhancement (0.1 mmol/kg) and diffuse myocardial fibrosis by T1 mapping using a modified Look-Locker pulse sequence measuring T1 and extracellular volume fraction (ECV).ResultsCFVR and CMR were performed in 64 women, mean (SD) age 62.5 (8.3) years. MBFR was performed in a subgroup of 54 (84 %) of these women. Mean native T1 was 1023 (86) and ECV (%) was 33.7 (3.5); none had focal fibrosis. Median (IQR) CFVR was 2.3 (1.9; 2.7), 23 (36 %) had CFVR < 2 indicating coronary microvascular disease, and median MBFR was 2.7 (2.2; 3.0) and 19 (35 %) had a MBFR value below 2.5. No significant correlations were found between CFVR and ECV or native T1 (R 2 = 0.02; p = 0.27 and R 2 = 0.004; p = 0.61, respectively). There were also no correlations between MBFR and ECV or native T1 (R 2 = 0.1; p = 0.13 and R 2 = 0.004, p = 0.64, respectively). CFVR and MBFR were correlated to hypertension and heart rate.ConclusionIn women with angina and no obstructive coronary artery disease we found no association between measures of coronary microvascular disease and myocardial fibrosis, suggesting that myocardial ischemia induced by coronary microvascular disease does not elicit myocardial fibrosis in this population. The examined parameters seem to provide independent information about myocardial and coronary disease.

Simultaneous multislice cardiac magnetic resonance fingerprinting using low rank reconstruction

“…With all cMRF scans, the T 2 measurements were consistent across all slice positions. cMRF T 1 measurements were slightly (20–50 ms) higher in basal slices compared with medial and apical slices; similar trends in T 1 from basal to apical slices have been reported elsewhere . A larger spread in T 1 and T 2 measurements was observed in basal slices for both cMRF (MB = 1 and MB = 3) and MyoMaps.…”

“…These scans required six separate breathholds (one per slice with T 1 and T 2 acquired separately) similar trends in T 1 from basal to apical slices have been reported elsewhere. 57,58 A larger spread in T 1 and T 2 measurements was observed in basal slices for both cMRF (MB = 1 and MB = 3) and MyoMaps. Figure 11 presents a similar analysis of the mean and standard deviation in T 1 and T 2 within the 16 AHA myocardial segments.…”

Coronary microvascular dysfunction and myocardial contractile reserve in women with angina and no obstructive coronary artery disease

“…Our research group has recently published a study showing no association between CFVR and focal or diffuse myocardial fibrosis assessed by cardiac magnetic resonance imaging in women with angina but no obstructive CAD included in the iPOWER study . This indicates that the reduced LV contractile reserve in patients with CMD is unlikely to be explained by increased myocardial stiffness (as also supported by the lack of association found between CFVR and LV diastolic dysfunction) and other factors probably play a predominant role, for example, a supply/demand mismatch of myocardial perfusion caused by CMD.…”

“…However, CMD and diastolic dysfunction could also be linked by shared underlying factors such as LV hypertrophy and fibrosis caused, for example, by hypertension and other cardiovascular risk factors . However, as mentioned a substudy of the iPOWER multicentre study showed no association between fibrosis and CMD . Thirdly, a high filling pressure could also affect the subendocardial tissue and thereby the microvasculature causing CMD.…”

“…35,36 However, as mentioned a substudy of the iPOWER multicentre study showed no association between fibrosis and CMD. 29 Thirdly, a high filling pressure could also affect the subendocardial tissue and thereby the microvasculature causing CMD. However, in the present study of patients with no obstructive CAD, we found no association between CMD and filling pressure.…”