Abnormalities of myocardial perfusion and glucose metabolism in patients with isolated left ventricular non-compaction

Gao, Xiao-Jin; Li, Yan; Kang, Lianming; Zhang, Jiän; Lü, Ming-De; Wan, Jian; Luo, Xiaoliang; He, Zhaoyi; Zhao, Shihua; Yang, Min-Fu; Yang, Yuejin

doi:10.1007/s12350-014-9890-8

Cited by 10 publications

(6 citation statements)

References 19 publications

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“…An arrest of myocardial compaction process leads to the inappropriate formation of coronary microvessels. A decreased myocardial perfusion in noncompacted areas has been shown in previous case reports and small studies, even though epicardial coronary arteries appear normal 2 , 10 . It is possible that perfusion deficit could, under exertion, lead to subendocardial ischemia, although no clear evidence of it has been shown yet.…”

Section: Discussionsupporting

confidence: 56%

Transendocardial CD34⁺ Cell Transplantation in Noncompaction Cardiomyopathy

et al. 2018

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Noncompaction cardiomyopathy is a rare congenital heart disorder characterized by an arrest of the myocardial compaction process. This results in the altered formation of coronary microvessels with a resulting decrease in myocardial perfusion. Transendocardial CD34+ cell transplantation has been shown to increase myocardial perfusion and function in patients with non-ischemic heart failure. In our first-in-man case study, we investigated the feasibility, safety and clinical effect of transendocardial CD34+ cell therapy in a patient with noncompaction cardiomyopathy.

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Section: Discussionsupporting

confidence: 56%

Transendocardial CD34⁺ Cell Transplantation in Noncompaction Cardiomyopathy

et al. 2018

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“…The hypothesis of myocardial ischemia has been given as explanation of the fibrosis 4,27,28 which is supported by the finding of a decline in myocardial perfusion in LVNC patents. 29, 30 We found the native T1 values in LVNC patients with and without LGE were significantly higher than in the normal controls. Similar findings were documented in previous studies of hypertrophic cardiomyopathy (HCM) and DCM.…”

Section: Disclosuresmentioning

confidence: 72%

Characterization of Compacted Myocardial Abnormalities by Cardiac Magnetic Resonance With Native T1 Mapping in Left Ventricular Non-Compaction Patients　– A Comparison With Late Gadolinium Enhancement –

Zhou

Xue

Fang

et al. 2016

Circ J

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Background: Native T1 mapping is an emerging cardiac magnetic resonance technique for quantitative evaluation of cardiomyopathies. This study aimed to investigate the usefulness of native T1 mapping in characterizing myocardial abnormalities in left ventricular non-compaction (LVNC) by comparing it with late gadolinium enhancement (LGE). Methods and Results:The study group of 31 LVNC patients and 8 normal controls underwent cardiovascular magnetic resonance to acquire the native T1 maps and LGE images. Of the 31 LVNC patients, 14 had LGE. The mean native T1 value of the normal controls, LGE(−) and LGE(+) patients was 1,098.8±40.8 ms, 1140.6±32.8 ms, and 1181.4±53.7 ms, respectively. Significant differences were found in native T1 between any 2 groups (F=9.74, P<0.001). In discriminating the presence of LGE in LVNC patients, the odds ratio and corresponding 95% confidence interval (CI) of native T1 were, respectively, 2.966 (95% CI: 1.123-7.835, P=0.028) and 4.348 (95% CI: 1.155-16.363, P=0.030) before and after adjusting for confounding factors with an increment of 1 standard deviation. Conclusions:The finding that LGE(−) patients had elevated native T1 compared with normal controls suggested native T1 mapping can be used earlier than LGE imaging to detect myocardial fibrosis in LVNC patients. Furthermore, higher native T1 values in LGE(+) patients than in the LGE(−) group suggested native T1 mapping is more sensitive than LGE imaging for identifying myocardial fibrosis in LVNC patients. 1211 Native T1 Mapping Evaluates Myocardium Abnormality factors for cardiac disease (diabetes mellitus, hypertension, and smoking) were enrolled as normal controls. The age and sex of the normal volunteers were matched with the LVNC patient group. Clinical information was collected from the medical record. The study protocol was approved by the local Institutional review board and written informed consent was given by all subjects. CMR ProtocolThe CMR imaging was performed with a 3.0-T MR system (Achieva TX, Philips Healthcare, Best, The Netherlands) using a 32-channel phased array heart coil (InVivo, Gainesville, FL, USA). The cine, phase-sensitive inversion recovery (PSIR), and modified look-locker inversion recovery (MOLLI) image sequences were acquired. 16 The ECG-gated balanced steadystate free precession (bSSFP) cine images of the long-and short-axis (SAX) images covering the entire LV were acquired with the following parameters: TR/TE 2.7/1.3 ms with 30 heart phases; voxel size 1.8×1.5×8.0 mm 3 ; slice thickness 8 mm; and slice spacing 2 mm. The PSIR sequence was acquired 15±5 min after the injection of 0.2 mmol/kg of gadolinium-DTPA (Magnetism, Bayer Schering Pharma, Guangzhou, China) with flow rate of 3 ml/s and 20 ml saline for flushing. The LGE images were obtained during mid-diastole in the same SAX orientations as cine, covering the whole LV, with the following imaging

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“…6 Similarly, Gao et al recently described myocardial perfusion abnormalities, as seen by myocardial SPECT, in patients with isolated NCM; however, no correlation between the extent of myocardial perfusion abnormalities and LVEF has been observed. 17 All authors speculated that myocardial perfusion abnormalities result from failure of coronary microcirculation growth and microcirculatory dysfunction. 6,16,17 A recent review by Towbin et al has also explained that the pathophysiological background of NCM could be subendocardial perfusion defects due to lack of small coronary blood vessels in the noncompacted area.…”

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confidence: 99%

“…17 All authors speculated that myocardial perfusion abnormalities result from failure of coronary microcirculation growth and microcirculatory dysfunction. 6,16,17 A recent review by Towbin et al has also explained that the pathophysiological background of NCM could be subendocardial perfusion defects due to lack of small coronary blood vessels in the noncompacted area. 3 Abnormalities were found to exist in noncompacted as well as compacted segments, suggesting than NCM is diffuse cardiomyopathy affecting also morphologically normal compacted myocardium.…”

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confidence: 99%

Impairment of myocardial perfusion correlates with heart failure severity in patients with non‐compaction cardiomyopathy

et al. 2020

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Aims Non-compaction cardiomyopathy (NCM) is a congenital heart disease characterized by an arrest of the myocardial compaction process. Although NCM patients have impaired formation of microvasculature, the functional impact of these changes remains undefined. We sought to analyse a potential correlation between myocardial ischemia and heart failure severity in NCM patients. Methods and resultsWe enrolled 41 NCM patients (28 male and 13 female), aged 21-70 years. In all patients, we have determined left ventricular end-diastolic volume (LVEDV), left ventricular ejection fraction (LVEF), and global longitudinal strain (GLS) by echocardiography. At the same time, serum levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) have been measured, and myocardial single-photon emission computed tomography at rest and on stress was used to define significant myocardial ischemia defined as summed difference score ≥ 2. Myocardial ischemia has been demonstrated in 11 patients (27%, Group A), and 30 patients showed no significant ischemic changes (73%, Group B). The groups did not differ in sex, age, kidney, or liver function. When compared with Group B, Group A had significantly lower LVEF (35 ± 15% in Group A vs. 53 ± 11% in Group B, P < 0.001), higher LVEDV (188 ± 52 mL vs. 136 ± 52 mL, P = 0.007), lower GLS (À9.9 ± 5.2% vs. À14.5 ± 4.1%, P = 0.001), and higher NT-proBNP levels (1691 ± 1883 pg/mL vs. 422 ± 877 pg/mL, P = 0.006). Overall, higher summed difference score was associated with lower LVEF (r = À0.48, P = 0.001), higher LVEDV (r = 0.39, P = 0.012), lower GLS (r = 0.352, P = 0.024), and higher levels of NT-proBNP (r = 0.66, P < 0.001).Conclusions The presence of myocardial ischemia in patients with NCM is associated with worse left ventricular function, dilation of the left ventricle, and more pronounced neurohumoral activation.

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Abnormalities of myocardial perfusion and glucose metabolism in patients with isolated left ventricular non-compaction

Abstract: In the current study, myocardial perfusion/metabolism mismatch and match were observed in both non-compacted and compacted myocardium in ILVNC patients. Further research is warranted to determine their pathologic and clinical significance.

Cited by 10 publications

References 19 publications

Transendocardial CD34⁺ Cell Transplantation in Noncompaction Cardiomyopathy

Transendocardial CD34⁺ Cell Transplantation in Noncompaction Cardiomyopathy

Characterization of Compacted Myocardial Abnormalities by Cardiac Magnetic Resonance With Native T1 Mapping in Left Ventricular Non-Compaction Patients　– A Comparison With Late Gadolinium Enhancement –

Impairment of myocardial perfusion correlates with heart failure severity in patients with non‐compaction cardiomyopathy

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Abnormalities of myocardial perfusion and glucose metabolism in patients with isolated left ventricular non-compaction

Abstract: In the current study, myocardial perfusion/metabolism mismatch and match were observed in both non-compacted and compacted myocardium in ILVNC patients. Further research is warranted to determine their pathologic and clinical significance.

Cited by 10 publications

References 19 publications

Transendocardial CD34+ Cell Transplantation in Noncompaction Cardiomyopathy

Transendocardial CD34+ Cell Transplantation in Noncompaction Cardiomyopathy

Characterization of Compacted Myocardial Abnormalities by Cardiac Magnetic Resonance With Native T1 Mapping in Left Ventricular Non-Compaction Patients – A Comparison With Late Gadolinium Enhancement –

Impairment of myocardial perfusion correlates with heart failure severity in patients with non‐compaction cardiomyopathy

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Transendocardial CD34⁺ Cell Transplantation in Noncompaction Cardiomyopathy

Transendocardial CD34⁺ Cell Transplantation in Noncompaction Cardiomyopathy

Characterization of Compacted Myocardial Abnormalities by Cardiac Magnetic Resonance With Native T1 Mapping in Left Ventricular Non-Compaction Patients　– A Comparison With Late Gadolinium Enhancement –