Subendocardial Involvement as an Underrecognized Cardiac MRI Phenotype in Myocarditis.

Background Subendocardial late gadolinium enhancement (LGE) detected with cardiac MRI in myocarditis represents a diagnostic dilemma, since it may resemble myocardial ischemia. Purpose To explore and compare the histopathologic characteristics and clinical features and outcomes in patients with myocarditis with and without subendocardial involvement at cardiac MRI. Materials and Methods This retrospective study evaluated 39 patients with myocarditis pathologically proven by means of either endomyocardial biopsy or explant pathologic findings between 2015 and 2020. Patients were divided into two groups according to cardiac MRI phenotype: 18 with subendocardial involvement (mean age ± standard deviation, 40 years ± 17; 10 women) and 21 with no subendocardial involvement (mean age, 35 years ± 11; six women). The median follow-up period was 784 days (interquartile range [IQR], 90-1123 days). The Student t test, Mann-Whitney U test, and univariable Cox regression were used for statistical analyses. Results In the 18 patients with subendocardial involvement, 12 (67%) had lymphocytic myocarditis and six (33%) had giant cell myocarditis. Patients with subendocardial involvement compared with those without subendocardial involvement had lower left ventricular ejection fraction (mean ± standard deviation, 27% ± 11 vs 41% ± 19; P = .004), larger LGE extent (median, 13% [IQR, 10%-22%] vs 5% [IQR, 2%-17%]; P < .001), higher rates of cardiac death or transplant (eight of 18 patients [44%] vs one of 21 patients [4.8%]; P = .006), higher probability of giant cell myocarditis (six of 18 [33%] vs one of 21 [4.8%]; P = .02), and more major adverse cardiovascular events (MACE) (15 of 18 [83%] vs seven of 21 [33%]; P = .002). In a subgroup of patients with comparable LGE extent (median, 15% vs 16%; P = .40) and left ventricular ejection fraction (median, 27% vs 31%; P = .26), the prognostic difference in terms of MACE remained (15 of 17 patients [88%] vs five of 10 [50%]; P = .02). Conclusion Subendocardial involvement detected with cardiac MRI in myocarditis indicated more severe clinical features, including a higher frequency of severe lymphocytic myocarditis or giant cell myocarditis and worse prognosis. © RSNA, 2021 See also the editorial by de Roos in this issue.

Evaluation of left ventricular volumes and ejection fraction by 99mTc-MIBI gated SPECT and 18F-FDG gated PET in patients with prior myocardial infarction.

BACKGROUND: This study aimed to compare the accuracy of gated-SPECT (GSPECT) and gated-PET (GPET) in the assessment of left ventricular (LV) end-diastolic volumes (EDVs), end-systolic volumes (ESVs) and LV ejection fractions (LVEFs) among patients with prior myocardial infarction (MI). METHODS: One hundred and sixty-eight consecutive patients with MI who underwent GSPECT and GPET were included. Of them, 76 patients underwent CMR in addition to the two imaging modalities. The measurements of LV volumes and LVEF were performed using Quantitative Gated SPECT (QGS), Emory Cardiac Toolbox (ECTB), and 4D-MSPECT (4DM). RESULTS: The correlation between GPET, GSPECT, and CMR were excellent for LV EDV (r = 0.855 to 0.914), ESV (r = 0.852 to 0.949), and LVEF (r = 0.618 to 0.820), as calculated from QGS, ECTB, and 4DM. In addition, subgroup analysis revealed that EDV, ESV, and LVEF measured by GPET were accurate in patients with different extents of total perfusion defect (TPD), viable myocardium, and perfusion/metabolic mismatch. Furthermore, multivariate regression analysis identified that mismatch score was associated with the difference in EDV (P < 0.05) measurements between GPET and CMR. CONCLUSIONS: In patients with MI, LV volumes and LVEF scores measured by both GSPECT and GPET imaging were comparable to those determined by CMR, but should not be interchangeable in individual patients.

Contributing Factor of Proximal Arch Dilation in Patients with Bicuspid Aortic Valve-Wall Shear Stress or Upward Extension of Ascending Aorta Dilation?

PURPOSE: The dilation of proximal arch (PArc) was suspected to develop as a result of valve-related hemodynamics or in consequence to the upward extension of the ascending aorta (AAo) dilation. We aimed to investigate the one that could be the possible contributing factor in patients with bicuspid aortic valve (BAV). METHODS: All enrolled BAV patients underwent four-dimensional flow magnetic resonance imaging. Contour-averaged circumferential wall shear stress (WSScirc,avg) and the diameter of the middle of AAo (mid-AAo) were compared between the patients with and without PArc dilation. Additionally, we analyzed the correlation between WSScirc,avg and aortic diameter at PArc section, as well as the correlation between the diameter of mid-AAo and that of PArc. RESULTS: No significant difference was observed in WSScirc,avg at PArc section between the patients with and without PArc dilation (P = .621). However, the diameter of mid-AAo in the patients who suffered PArc dilation was higher than those without it (P = .007). In addition, the aortic diameter did not correlate with the WSScirc,avg at PArc level (R = -0.068, P = .701). The correlation was observed between PArc diameter and mid-AAo diameter (R = 0.521, P = .002). CONCLUSION: Hemodynamics may not contribute to the development of PArc dilation. PArc diameter correlated with mid-AAo diameter, indicating PArc dilation may be secondary to the upward extension of AAo dilation. The influence of AAo dilation extending upward could be treated by AAo replacement; hence, a selective approach to transverse PArc replacement might be appropriate.

Microglia activation induces oxidative injury and decreases SIRT3 expression in dopaminergic neuronal cells.

Microglia activation-mediated neuroinflammation plays an important role in the progression of Parkinson's disease (PD). However, effects of microglia activation on dopaminergic neuronal cell (DAC) fate are still poorly understood. The objective of this study was to explore the neurotoxic effects of microglia activation-mediated oxidative injury in DACs and its possible mechanisms. In the present study, microglia-DACs co-culture systems (murine BV-2 and MN9D cells, or primary microglia and mesencephalic neurons) were used to display the crosstalk between both cell types. The cytotoxicity of lipopolysaccharide-induced microglia activation led to the accumulation of intracellular reactive oxygen species, increased cell apoptosis rate, reduced number of DACs, concomitant to cell cycle arrest at G1 phase. Molecular mechanisms of apoptosis caused by microglia activation-induced oxidative injury included the increased opening of mitochondrial permeability transition pore and enhanced membrane potential depolarization in MN9D cells, down-regulation of Bcl-2 and up-regulation of Bax, caspase-3 expression in DACs. In addition, microglia activation made a significant reduction of SIRT3 and superoxide dismutase 2 gene expression in DACs. Taken together, these data imply that microglia activation promotes cell apoptosis through mitochondrial pathway and decreases SIRT3 expression in DACs, which may provide some support for PD progression promoted by neuroinflammation.

Relationship of myocardial hibernation, scar, and angiographic collateral flow in ischemic cardiomyopathy with coronary chronic total occlusion.

BACKGROUND: The relationship between myocardial viability and angiographic collateral flow is not fully elucidated in ischemic cardiomyopathy (ICM) with coronary artery chronic total occlusion (CTO). We aimed to clarify the relationship between myocardial hibernation, myocardial scar, and angiographic collateral flow in these patients. METHODS AND RESULTS: Seventy-one consecutive ICM patients with 122 CTOs and 652 dysfunctional segments within CTO territories were retrospectively analyzed. Myocardial hibernation (perfusion-metabolism mismatch) and the extent of 18F-fluorodeoxyglucose (FDG) abnormalities were assessed using 99mTc-sestamibi and 18F-FDG imaging. Myocardial scar was evaluated by late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) imaging. Collateral flow observed on coronary angiography was assessed using Rentrop classification. In these patients, neither the extent nor frequency of myocardial hibernation or scar was related to the status of collateral flow. Moreover, the matching rate in determining myocardial viability was poor between any 2 imaging indices. The extent of 18F-FDG abnormalities was linearly related to the extent of LGE rather than myocardial hibernation. Of note, nearly one-third (30.4%) of segments with transmural scar still had hibernating tissue. Hibernation and non-transmural scar had higher sensitivity (63.0% and 66.7%) than collateral flow (37.0%) in predicting global functional improvement. CONCLUSIONS: Angiographic collateral cannot accurately predict myocardial viability, and has lower sensitivity in prediction of functional improvement in CTO territories in ICM patients. Hence, assessment of myocardial viability with non-invasive imaging modalities is of importance. Moreover, due to the lack of correlation between myocardial hibernation and scar, these two indices are complementary but not interchangeable.

The impacts of severe perfusion defects, akinetic/dyskinetic segments, and viable myocardium on the accuracy of volumes and LVEF measured by gated 99mTc-MIBI SPECT and gated ¹8F-FDG PET in patients with left ventricular aneurysm: cardiac magnetic resonance imaging as the reference.

BACKGROUND: To compare the accuracy of end-diastolic and end-systolic volumes (EDV, ESV) and LV ejection fraction (LVEF) measured by both GSPECT and GPET, using cardiac magnetic resonance imaging (CMR) as a reference. Furthermore, the impacts of severe perfusion defects, akinetic/dyskinetic segments, and residual viable myocardium on the accuracy of LV functional parameters were investigated. METHODS: Ninety-six consecutive patients with LV aneurysm and LV dysfunction (LVEF 32 ± 9%) diagnosed by CMR were studied with GSPECT and GPET. EDV, ESV, and LVEF were calculated using QGS software. RESULTS: Correlations of volumes were excellent (r 0.81-0.86) and correlation of LVEF was moderate (r 0.65-0.76) between GSPECT vs CMR and between GPET vs CMR. Compared with CMR, ESV was overestimated by GSPECT (P < .01) and underestimated by GPET (P < .0001); EDV was underestimated by GPET (P < .001); LVEF was underestimated by GSPECT but overestimated by GPET (both P < .001). Multivariate regression analysis revealed that the number of segments with severe perfusion defects (P < .001) was the only independent factor which was correlated to the EDV difference between GSPECT and CMR, the number of akinetic/dyskinetic segments with absent wall thickening (WT) was the only independent factor which was significantly correlated to the differences of ESV and LVEF measurements between GSPECT vs CMR and between GPET vs CMR (P < .0001), respectively. Neither the mismatch score nor the segments with viable myocardium were correlated to the differences of LV volumes and LVEF measurements between different imaging modalities. CONCLUSIONS: In LV aneurysm patients, LV volumes and LVEF measured by both GSPECT and GPET imaging correlated well with those determined by CMR, but should not be interchangeable in individual patients. The accuracy of LVEF measured by GSPECT and GPET was affected by the akinetic/dyskinetic segments with absent WT.

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

BACKGROUND: The prevalence of myocardial perfusion and glucose metabolic abnormalities and their significance in patients with isolated left ventricular non-compaction (ILVNC) have not been well investigated. METHODS: Seventeen ILVNC patients who underwent cardiac magnetic resonance (CMR) and (99m)Tc-sestamibi SPECT/fluorine-18 deoxyglucose ((18)F-FDG) PET imaging were included. Left ventricular non-compaction, regional wall motion abnormalities, left ventricular ejection fraction (LVEF), and delayed enhancement (DE) were estimated using CMR. Myocardial perfusion and metabolism were evaluated with SPECT/PET. RESULTS: Ninety-five (32.9%) segments were considered non-compacted. DE was present in 52 (18.0%) segments and 10 (58.8%) patients. The rate of occurrence of DE was significantly higher in compacted segments than in non-compacted segments (22.7% vs 8.4%, P = .003). Myocardial perfusion abnormalities were present in 92 (31.8%) segments, of which 66 were perfusion/metabolism match and 26 were perfusion/metabolism mismatch. The rate of occurrence of perfusion abnormality was similar between compacted and non-compacted segments (32.0% vs 31.6%, P = .948), but it was significantly higher in segments with DE than in those without DE (51.9% vs 27.4%, P = .001). None of the imaging features alone (non-compaction, DE, perfusion abnormalities, match or mismatch) showed significant correlations with LVEF (all P > .05). CONCLUSION: 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.

Apical aneurysm formation in apical hypertrophic cardiomyopathy: Pilot study with cardiac magnetic resonance.

BACKGROUND: The dynamic changes and apical aneurysm formation in apical hypertrophic cardiomyopathy (HCM) have not been specifically described. This study aimed to describe these changes to better understand the progression of apical HCM. METHODS AND RESULTS: Seventy-two patients with apical HCM who underwent at least two cardiac magnetic resonance (CMR) examinations were retrospectively included in this study. The mean interval between the first and last CMR examinations was 50.1 ± 26.8 months (ranging from 4 to 118 months). Compared with the initial values, the left atrial diameter, maximum left ventricular wall thickness and late gadolinium enhancement extent significantly increased (all P < 0.05), while the left ventricular ejection fraction significantly decreased (P < 0.05), at the latest CMR examination. More importantly, the dynamic process of apical aneurysm formation in apical HCM was observed in a subset of patients, which may follow these four stages: starting with systolic apical cavity obliteration, then broadening of the apical slit in systole, further developing into an apical outpouching, and finally forming an apical aneurysm. Eleven patients experienced adverse cardiovascular events, including new-onset or progressive atrial fibrillation (n = 7), hospitalization with heart failure (n = 3) and implantable cardioverter defibrillator intervention (n = 1), at the time of the latest CMR examination. CONCLUSIONS: In the progression of apical HCM, cardiac structure and function will change accordingly. Apical aneurysm formation in apical HCM is a chronic and continuous dynamic process that may follow a 4-step pathway of disease progression.

[The correlation between BRAF mutations, RET/PTC rearrangements and platelet-derived growth factor B expression in papillary thyroid carcinomas].

OBJECTIVE: To investigate the prevalence of BRAF T1799A mutation and RET/PTC rearrangement in Qingdao and detect the expression of platelet-derived growth factor B (PDGF-B) in order to investigate the correlation between gene mutation and PDGF-B. METHODS: Fresh tissue from 48 papillary thyroid carcinomas (PTC) patients was examined for BRAF mutation RET rearrangements (RET/PTC1 and RET/PTC3) by PCR, followed by direct-sequence analysis. The expression of PDGF was analyzed by immunohistochemistry. RESULTS: Among the 48 patients, 14 (29.2%) were micro PTC; 18 (37.5%) had BRAF T1799A mutations and 23(47.9%) had RET/PTC rearrangement. There were 17 (35.4%) cases of RET/PTC1 and 6 (12.5%) of RET/PTC3, with no multiple rearrangements. Both BRAF T1799A mutation and RET/PTC rearrangement were present in 6 (12.5%) cases of non-micro PTC. The level of PDGF-B expression in BRAF T1799A positive was higher than that in the negative, and the level of PDGF-B expression in RET/PTC3 was higher than that in RET/PTC1 (P < 0.05). The more advanced neoplasm stage was, the stranger PDGF-B expression was. CONCLUSIONS: The incidence of BRAF T1799A mutation and RET/PTC rearrangement is higher in Qingdao. BRAF T1799A mutation and RET/PTC3 rearrangement in patients suggests a poorer prognosis than the negative one. The BRAF T1799A mutation and RET/PTC3 rearrangement may strengthen the expression of PDGF-B. Both variations suggest a poor prognosis.

[Clinical and cardiac imaging characteristics of patients with left ventricular apical hypoplasia].

OBJECTIVE: To analyze the clinical and cardiac imaging characteristics of patients with left ventricular apical hypoplasia (LVAH). METHODS: From January 2008 to January 2012, seven patients [3 male/4 female, age: 6 - 44 (19.9 ± 14.2) years] with LVAH were included in this cohort. Transthoracic echocardiogram was performed in all patients, cardiovascular MRI was performed in 3 patients and cardiovascular CT in another 2 patients. In addition, one LVAH patient underwent cardiac catheterization and angiography examination. RESULTS: Four out of 7 patients complained chest discomfort. Precordial murmur was heard in 3 patients. Atrial fibrillation was evidenced by electrocardiogram in 3 patients. Left ventricular end-diastolic diameter [(57.9 ± 11.6) mm] increased while left ventricule (LV) longitudinal diameter reduced in all patients. Left ventricular systolic function was reduced in 2 patients and mean LVEF was (47.6 ± 17.2)%. The interventricular septum bulged towards the right, and the ventricular septum thickness was (7.3 ± 1.2) mm. The papillary muscles were dominant on the flattened LV anteroapical region. The right ventricle elongated and wrapped around the hypoplastic left ventricular apex, and the dimension of right ventricle was (19.7 ± 7.6) mm. Focal fat replacement of the left ventricular apical wall was evidenced in 5 patients underwent cardiovascular MRI or CT examinations. CONCLUSIONS: Clinical symptoms are non-specific in LVAH patients. Truncated and spherical LV, abnormal origin of papillary muscles in the flattened LV anterior apex and an elongated right ventricle wrapping around the LV apex as well as focal fat replacement of the left ventricular apical wall are typical imaging characteristics of LVAH.

Utility of cardiac magnetic resonance in the diagnosis of suspected "MINOCA": a case series and literature review.

Myocardial infarction with nonobstructive coronary artery (MINOCA) is a common condition in clinical practice with multiple specific causes, such as plaque rupture, plaque erosion, and epicardial coronary vasospasm. There must be an ischemic mechanism responsible for the myocyte injury and an exclusion of nonischemic mechanisms that can mimic myocardial infarction, and then a diagnosis of MINOCA can be made. Cardiac magnetic resonance (CMR) plays an essential role in the diagnosis and differential diagnosis of MINOCA, which cannot only exclude myocarditis, Takotsubo syndrome, and cardiomyopathies, but also provide imaging confirmation of acute myocardial infarction. In this study, we presented 2 typical cases with the clinical presentation of acute myocardial infarction but normal or nonobstructive epicardial coronary arteries. Further CMR examinations showed different patterns of late gadolinium enhancement (LGE) in these 2 cases, one case with subendocardial LGE of the anterolateral wall and the other one with subepicardial LGE of the lateral wall, which indicated 2 different mechanisms for the myocyte injury. Subsequently, these 2 patients received different treatment regimens and were discharged with improved symptoms. In conclusion, CMR should be a mandatory test in patients with suspected MINOCA, because it can not only make a clear diagnosis, but also play an important role in guiding clinical decision-making.

SIRT3 expression alleviates microglia activation­induced dopaminergic neuron injury through the mitochondrial pathway.

The mitochondrial protein sirtuin 3 (SIRT3) can counteract cell damage caused by oxidative stress and inflammation, and contribute to cell survival primarily by improving mitochondrial function. However, the effects of SIRT3 in dopaminergic neuronal cells (DACs) remain unclear. In our previous studies, microglia activation-associated cytotoxicity was observed to promote the apoptosis of DACs, along with the decrease of SIRT3 expression. The aim of the present study was to explore the potential neuroprotective effect of SIRT3 expression against dopaminergic neuron injury caused by microglia activation, and clarify its possible mechanisms. SIRT3 overexpression in DACs reduced the production of intracellular reactive oxygen species (ROS), cell apoptosis rate, mitochondrial membrane potential (ΔΨm) depolarization, opening of mitochondrial permeability transition pore (mPTP) and cyclophilin D (CypD) protein level, and promoted cell cycle progression. However, SIRT3 siRNA-mediated knockdown further aggravated microglia activation-mediated cytotoxicity, including ROS accumulation, increased cell apoptosis and mPTP opening, elevated the CypD level, enhanced mitochondrial ΔΨm depolarization, concomitant to cell cycle arrest at G0/G1 phase. The mechanisms of SIRT3 mitigated microglia activation-induced DAC dysfunction, which included decreased mPTP opening and Bax/Bcl-2 ratio, inhibition of mitochondrial cytochrome c release to the cytoplasm, reduced caspase-3/9 activity, increased LC3II/LC3I and beclin-1 protein expression levels, and decreased nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing protein 3 (NLRP3), caspase-1, IL-1ß and IL-18 protein expression. In conclusion, these results indicated that SIRT3 expression attenuated cell damage caused by microglia activation through the mitochondrial apoptosis pathway in DACs. The mitophagy-NLRP3 inflammasome pathway may also be associated with this neuroprotection. These findings may provide new intervention targets for the survival of dopaminergic neurons and the prevention and treatment of Parkinson's disease.

[Clinical characteristics of fat replacement of left ventricular myocardium].

OBJECTIVE: To evaluate the clinical characteristics of left ventricular fat replacement. METHODS: We identified 45 patients [28M/17F, mean age (51.9 ± 14.7) years] with left ventricular myocardial fat replacement (CT value ≤ -30 Hu) by cardiovascular CT. RESULTS: Among 45 patients, 25 patients [20M/5F, mean age (61.2 ± 10.4) years]were diagnosed as coronary artery disease (CAD). There was 56%single-vessel disease, 20% double-vessel disease and 24%triple-vessel disease, true left ventricular aneurysm was detected in 3 patients and left ventricular thrombi in 1 patient, the dimension of left ventricle was (54.5 ± 9.4) mm and the LVEF was (51.8 ± 13)% in CAD group. In this group, fat replacement occurred in the region of myocardial infarction and presented as curvilinear band in subendocardial region. The left ventricular wall thickness was lower than 5 mm in 21 cases. The location of fat replacement in CAD group is as follows: apical region in 18 patients, distal septal in 15 patients, distal anterior in 11 patients, mid-septal in 7 patients, mid-anterior in 7 patients and basal in 1 patients. The age of remaining 20 patients (8M/12F) without CAD were (57.8 ± 13.3) years. In the group of non-CAD, dilated cardiomyopathy was diagnosed in 3 patients, atrial septal defect in 1 patient, rheumatic heart disease in 1 patient, there was no structural heart disease in the remaining 15 patients. The dimension of left ventricle was (51.1 ± 9.1) mm and the LVEF was (59.4 ± 13.9)%. In non-CAD group, fat replacement mainly occurred in septal region, presented as curvilinear band in 17 patients and patch in 3 patients. The location of fat replacement in this group is as follows: mid-septal region in 11 patients, distal-septal in 10 patients and apical in 9 patients. The intramural fat replacement was detected in 14 patients: subendocardial fat replacement in 10 patients and both intramural and subendocardial fat replacement in 4 patients. CONCLUSIONS: Left ventricular fat replacement could be documented in CAD patients, non-CAD cardiomyopathy patients and in patients without structural heart disease. Left ventricular fat replacement often positioned in apical region in CAD patients as a consequence of infarct healing while mostly positioned in septal region in non-CAD patients, the definite clinical implication of left ventricular fat replacement in non-CAD patients remains to be clarified.

[Differentiation of true from false left ventricular aneurysm with magnetic resonance imaging in patients after myocardial infarction].

OBJECTIVE: To observe the value of cardiac magnetic resonance imaging (MRI) for differentiation of true from false left ventricular aneurysm in patients after myocardial infraction (MI). METHODS: Twenty-six patients [22 males/4 females, mean age (59.3 ± 9.3) years] with left ventricular aneurysm after MI were imaged with MRI, echocardiography and coronary angiography. The respective findings were compared with surgical pathology results. RESULTS: There were 24 patients with dyspnea and 15 patients with hypertension. LVEF measured by echocardiography was 36.9% ± 9.1% in this patient cohort. Cardiac MRI showed that the left ventricular end diastolic wall thickness was thinner than 5.5 mm in 24 cases, and between 5.5 to 8 mm in 2 cases. The dimension of left ventricle was (67.8 ± 9.3) mm. Dyskinesia presented in 24 cases, and akinesia in 2 cases. Delayed enhancement was shown in all cases by MRI. Cardiac MRI detected left ventricular true aneurysm in 23 cases, false aneurysm in 3 case and left ventricular thrombi in 7 cases. The diagnosis by magnetic resonance imaging corresponded well to pathological findings. Echocardiography misdiagnosed pseudoaneurysm in 1 patient, and failed to detected left ventricular thrombi in 2 cases. CONCLUSION: Cardiac MRI could correctly differentiate true from false left ventricular aneurysm in patients after MI.

[Incidence of coronary artery disease and outcome of patients with left ventricular noncompaction].

OBJECTIVE: To analyze the incidence of coronary artery disease (CAD) and outcome of patients with left ventricular noncompaction (LVNC). METHODS: Fifty-one patients with LVNC evaluated by echocardiography and/or cardiac magnetic resonance (CMR) from January 2006 to August 2010 were retrospectively reviewed. Coronary angiography or MDCT was performed for detecting coronary artery disease. Predictors of the cardiac events were analyzed by Cox regression analysis. RESULTS: There were 31 LVNC patients without CAD and 20 LVNC patients with CAD including single vessel coronary disease in 9 cases, double vessel coronary disease in 3 cases, three vessel coronary disease in 5 cases and left main coronary disease in 3 cases. Coronary artery bypass graft and percutaneous coronary intervention (PCI) were performed in 4 patients. Compared to LVNC patients without CAD, mean age (P = 0.008), incidence of hypertension (65.0% vs. 19.4%, P = 0.001), diabetes mellitus (40.0% vs. 12.9%, P = 0.026) and hyperlipidemia (55.0% vs. 25.8%, P = 0.035) were significantly higher while NT-proBNP level was significantly lower (P = 0.049) in LVNC patients with CAD. Incidence of major cardiac events was similar in LVNC patients with or without CAD. LogNT-proBNP is the independent prognostic factor for adverse cardiac events in patients with LVNC (HR 3.993, 95%CI 1.140 - 13.988, P = 0.030). CONCLUSIONS: Coronary artery disease is common in patients with LVNC and associated with traditional risk factors for CAD. Poor prognosis is associated with increased NT-proBNP but not with CAD in this patient cohort.

[Value of cardiac CT examination in middle-aged and elderly patients with atrial septal defect before planned transcatheter closure].

OBJECTIVE: To investigate the value of the cardiac CT examination for decision making in middle-aged and elderly patients before planned transcatheter atrial septal defect (ASD) closure. METHODS: Cardiac CT was performed in 63 adult patients [18 males, aged from 50 to 77 years, mean age (56.87 ± 5.79) years] with ASD before planned transcatheter ASD closure. Coronary CT angiography was made for detection of associated cardiovascular diseases, followed by 3D reconstruction of ASD for determination of the defect size in the GE-workstation, results were compared between transthoracic echocardiography measurement, CT measurement, and atrial septal defect occluder waist diameter. RESULTS: Cardiac CT identified additional cardiovascular diseases in 14 patients and decision making was changed based on cardiac CT results. Coronary artery stenosis was detected in 8 patients by cardiac CT, and proved by coronary angiography, and all of them were given comprehensive management: percutaneous coronary intervention and transcatheter ASD closure were successively performed in 2 cases, and 1 case was referred to surgery for both coronary artery bypass graft and surgical ASD repair, and 5 patients were given pharmacological management for coronary artery disease besides transcatheter ASD closure. Cardiac CT identified large ASD with insufficient rim tissue in 2 cases and transcatheter closures were abandoned. Cardiac CT screened out 1 case from those with insufficient posterior inferior rim by transthoracic echocardiography, and transcatheter ASD closure was successfully performed. Cardiac CT ruled out ASD in 1 patient. In addition, cardiac CT detected 1 partial abnormal pulmonary vein connection and 1 ductus arteriosus in this cohort. A correlation on ASD measurements was found between CT size and TTE size (r = 0.80, P < 0.01; Y = 0.84X + 8.85, R(2) = 0.63, P < 0.05), and between ASO size and CT size (r = 0.92, P < 0.01;Y = 0.93X + 4.78, R(2) = 0.84, P < 0.05). CONCLUSION: In middle-aged and elderly patients with ASD for possible transcatheter closure, cardiac CT is valuable on determine ASD size and morphology and could provide incremental information for optimizing clinical management for ASD patients.

Efficacy and safety of a parylene-coated occluder for atrial septal defect: a prospective, multi-center, randomized controlled clinical trial.

BACKGROUND: Nitinol-containing devices are widely used in clinical practice. However, there are concerns about nickel release after nitinol-containing device implantation. This study aimed to compare the efficacy and safety of a parylene-coated occluder vs. a traditional nitinol-containing device for atrial septal defect (ASD). METHODS: One-hundred-and-eight patients with ASD were prospectively enrolled and randomly assigned to either the trial group to receive a parylene-coated occluder (n = 54) or the control group to receive a traditional occluder (n = 54). The plugging success rate at 6 months after device implantation and the pre- and post-implantation serum nickel levels were compared between the two groups. A non-inferiority design was used to prove that the therapeutic effect of the parylene-coated device was non-inferior to that of the traditional device. The Cochran-Mantel-Haenszel chi-squared test with adjustment for central effects was used for the comparison between groups. RESULTS: At 6 months after implantation, successful ASD closure was achieved in 52 of 53 patients (98.11%) in both the trial and control groups (95% confidence interval (CI): [-4.90, 5.16]) based on per-protocol set analysis. The absolute value of the lower limit of the 95% CI was 4.90%, which was less than the specified non-inferiority margin of 8%. No deaths or severe complications occurred during 6 months of follow-up. The serum nickel levels were significantly increased at 2 weeks and reached the maximum value at 1 month after implantation in the control group (P < 0.05 vs. baseline). In the trial group, there was no significant difference in the serum nickel level before vs. after device implantation (P > 0.05). CONCLUSIONS: The efficacy of a parylene-coated ASD occluder is non-inferior to that of a traditional uncoated ASD occluder. The parylene-coated occluder prevents nickel release after device implantation and may be an alternative for ASD, especially in patients with a nickel allergy.

[Effects of left ventricular reconstruction on magnetic resonance imaging derived left ventricular wall stress and contractive function in patients with postinfarction ventricular aneurysm].

OBJECTIVE: To evaluate the effects of left ventricular reconstruction on left ventricular wall stress and function in patients with postinfarction left ventricular aneurysm. METHODS: During January 2005 to June 2006, 16 patients [15 male, (56.6 +/- 8.8) years] with postinfarction ventricular aneurysm received left ventricular reconstruction operation on CPB (5 linear repair, 6 endoventricular purse-string suture, 5 endoventricular patch repair) and CABG was also performed in 15 patients. MRI examination was made before and 3 months post operation by Siemens Magnetom Avanto 1.5T MR with routine cine-MRI in combination with late-delayed enhancement sequence. Left ventricular geometric parameters and segmental thickening were obtained with accessory image analysis software. Non-invasive blood pressure was acquired in order to compute ventricular wall stress. The revascularized and unrevascularized segments were defined by comparing the post operation revascularization of the blood-supply coronary artery with preoperative results. RESULTS: A total of 192 segments including 74 unrevascularized segments were analyzed. Segmental thickening were significantly increased while wall stress were significantly reduced in both unrevascularized and revascularized segments 3 months post operation compared to preoperative values (all P < 0.05). The increase of wall thickening was positively correlated with the reduction of wall stress in these segments. CONCLUSION: Left ventricular reconstruction plus CABG is associated with reduced left ventricular wall stress and increased myocardial contractive function in patients with postinfarction left ventricular aneurysm.