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Low coronary perfusion pressure is associated with endocardial fibrosis in a rat model of volume overload cardiac hypertrophy
Guido, Maria Carolina;Koike, Márcia Kiyomi;Frimm, Clovis de Carvalho;
Revista do Hospital das Clínicas , 2004, DOI: 10.1590/S0041-87812004000500002
Abstract: left ventricular hypertrophy following volume overload is regarded as an example of cardiac remodeling without increased fibrosis accumulation. however, infarction is associated with increased fibrosis within the noninfarcted, hypertrophied myocardium, particularly in the subendocardial regions. it is conceivable to suppose that, as also occurs postinfarction, low coronary driving pressure may also interfere with accumulation of myocardial fibrosis following aortocaval fistula. purpose: to investigate the role of acute hemodynamic changes in subsequent deposition of cardiac fibrosis in response to aortocaval fistula. method: aortocaval fistula were created in 4 groups of wistar rats that were followed over 4 and 8 weeks: aortocaval fistula 4 and aortocaval fistula 8 (10 rats each) and their respective controls (sham-operated controls - sh), sh4 and sh8 (8 rats each). hemodynamic measurements were performed 1 week after surgery. hypertrophy and fibrosis were quantified by myocyte diameter and collagen volume fraction at the end of follow up. result: compared with sh4 and sh8, pulse pressure, left ventricular end-diastolic pressure, and +dp/dt were higher in aortocaval fistula 4 and aortocaval fistula 8, but -dp/dt was similar. coronary driving pressure (mm hg), used as an estimate of perfusion pressure, was lower in aortocaval fistula 8 (52.6 ± 4.1) than in sh8 (100.8 ± 1.3), but comparable between aortocaval fistula 4 (50.0 ± 8.9) and sh4 (84.8 ± 2.3). myocyte diameter was greater in aortocaval fistula 8, whereas interstitial and subendocardial fibrosis were greater in aortocaval fistula 4 and aortocaval fistula 8. coronary driving pressure correlated inversely and independently with subendocardial fibrosis (r2 = .86, p <.001), whereas left ventricular systolic pressure (r2 = 0.73, p = .004) and end-diastolic pressure (r2 = 0.55, p = 012) correlated positively and independently with interstitial fibrosis. conclusion: coronary driving pressure falls and ventricular p
Correlation between reciprocal changes in eletrocardiogram of the patients with acute myocardial infarction and involvement of coronary artery that perfuse area of myocardium related to reciprocal changes
Nematipour E,Asgharnia Z
Tehran University Medical Journal , 2002,
Abstract: Introduction: Reciprocal changes are ST depression ≥1 mm in electrocardiogram of the patients with acute myocardial infarction in the reciprocal leads. This question that these changes are merely secondary to ST elevation in infarction area or that they are truly subendocardial ischemia secondary to involvement of coronary artery that perfuse that area is not clearly defined. Methods and Materials: In this study, 33 patients with acute myocardial infarction and reciprocal changes in ECG at the time of admission, were selected and coronary angiography was performed in them in a week of infarction. Results: Correlation between reciprocal changes in ECG and involvement of reciprocal coronary artery the coronary artery that perfuse area of myocardium related to reciprocal changes in ECG were studied. 32-63 percent of patients (1/3-2/3) with reciprocal changes had significant stenosis of reciprocal coronary artery in coronary angiography (CI=95 percent). The incidence of multivessel disease was about 60.6 percent. After coronary angiography 33.3 percent of patients referred for coronary arteries bypass graft surgery (CABGS) and 27.3 percent for percutaneous transluminal coronary artery angioplasty (PTCA). In the other words, 60.6 percent of our patients refered for revascularization, PTCA or CABGS. Conclusion: We concluded that because of the need for intervention in about 60 percent of our patients, coronary angiography could be recommended in all patients with acute myocardial infarction and reciprocal changes in ECG.
Subendocardial Fibrosis in Left Ventricular Hypertrabeculation-Cause or Consequence?
J. Ker, L. Du Toit-Prinsloo, W.F.P. Van Heerden and G. Saayman
Clinical Medicine Insights: Cardiology , 2012, DOI: 10.4137/CMC.S6507
Abstract: Left ventricular noncompaction has been classified as a primary cardiomyopathy with a genetic origin. This condition is morphologically characterized by a thickened, two-layered myocardium with numerous prominent trabeculations and deep, intertrabecular recesses. Recently, it has become clear that these pathological characteristics extend across a continuum with left ventricular hypertrabeculation at one end of the spectrum. The histological findings include areas of interstitial fibrosis. We present a case of left ventricular hypertrabeculation which presented as sudden infant death syndrome. Histologically areas of subendocardial fibrosis was prominent and we propose that this entity may be a hidden cause of arrhythmic death in some infants presenting as sudden infant death syndrome., with areas of subendocardial fibrosis as possible arrhythmogenic foci.
Subendocardial contractile impairment in chronic ischemic myocardium: assessment by strain analysis of 3T tagged CMR
Michinobu Nagao, Masamitsu Hatakenaka, Yoshio Matsuo, Takeshi Kamitani, Ko Higuchi, Fumiaki Shikata, Mitsugi Nagashima, Teruhito Mochizuki, Hiroshi Honda
Journal of Cardiovascular Magnetic Resonance , 2012, DOI: 10.1186/1532-429x-14-14
Abstract: 3T tagged CMR was performed at rest in 12 patients with severe coronary artery disease who had been scheduled for coronary artery bypass grafting. Circumferential strain (C-strain) at end-systole on subendocardial and epicardial layers was measured using the short-axis tagged images of the LV and available software (Intag; Osirix). The myocardial segment was divided into stenotic and non-stenotic segments by invasive coronary angiography, and ischemic and non-ischemic segments by stress myocardial perfusion scintigraphy. The difference in C-strain between the two groups was analyzed using the Mann-Whitney U-test. The diagnostic capability of C-strain was analyzed using receiver operating characteristics analysis.The absolute subendocardial C-strain was significantly lower for stenotic (-7.5 ± 12.6%) than non-stenotic segment (-18.8 ± 10.2%, p < 0.0001). There was no difference in epicardial C-strain between the two groups. Use of cutoff thresholds for subendocardial C-strain differentiated stenotic segments from non-stenotic segments with a sensitivity of 77%, a specificity of 70%, and areas under the curve (AUC) of 0.76. The absolute subendocardial C-strain was significantly lower for ischemic (-6.7 ± 13.1%) than non-ischemic segments (-21.6 ± 7.0%, p < 0.0001). The absolute epicardial C-strain was also significantly lower for ischemic (-5.1 ± 7.8%) than non-ischemic segments (-9.6 ± 9.1%, p < 0.05). Use of cutoff thresholds for subendocardial C-strain differentiated ischemic segments from non-ischemic segments with sensitivities of 86%, specificities of 84%, and AUC of 0.86.Analysis of tagged CMR can non-invasively demonstrate predominant impairment of subendocardial strain in the chronic ischemic myocardium at rest.Systolic wall thickening of the left ventricle (LV) is distributed transmurally inhomogeneously. In the normal myocardium, subendocardial deformation becomes markedly greater than subepicardial deformation [1]. The progression of myocardial ischemia ha
Transmural Heterogeneity of Myofilament Function and Sarcomeric Protein Phosphorylation in Remodeled Myocardium of Pigs with a Recent Myocardial Infarction  [PDF]
Jolanda van der Velden,Ger J. M. Stienen,Dirk J. Duncker
Frontiers in Physiology , 2011, DOI: 10.3389/fphys.2011.00083
Abstract: Aim: Transmural differences in sarcomeric protein composition and function across the left ventricular (LV) wall have been reported. We studied in pigs sarcomeric function and protein phosphorylation in subepicardial (EPI) and subendocardial (ENDO) layers of remote LV myocardium after myocardial infarction (MI), induced by left circumflex coronary artery ligation. Methods: EPI and ENDO samples were taken 3 weeks after sham surgery (n = 12) or induction of MI (n = 12) at baseline (BL) and during β-adrenergic receptor (βAR) stimulation with dobutamine. Isometric force was measured in single cardiomyocytes at various [Ca2+] and 2.2 μm sarcomere length. Results: In sham hearts, no significant transmural differences were observed in myofilament function or protein phosphorylation. Myofilament Ca2+-sensitivity was significantly higher in both EPI and ENDO of MI compared to sham hearts. Maximal force was significantly reduced in MI compared to sham, but solely in ENDO cells. A higher passive force was observed in MI hearts, but only in EPI cells. The proportion of stiff N2B isoform was higher in EPI than in ENDO in both sham and MI hearts, and a trend toward increased N2B-proportion appeared in MI EPI, but not MI Endo. Analysis of myofilament protein phosphorylation did not reveal significant transmural differences in phosphorylation of myosin binding protein C, desmin, troponin T, troponin I (cTnI), and myosin light chain 2 (MLC-2) both at BL and during βAR stimulation with dobutamine infusion. A significant increase in MLC-2 phosphorylation was observed during dobutamine only in sham. In addition, the increase in cTnI phosphorylation upon dobutamine was twofold lower in MI than in sham. Conclusion: Myofilament dysfunction is present in both EPI and ENDO in post-MI remodeled myocardium, but shows a high degree of qualitative heterogeneity across the LV wall. These heterogeneous transmural changes in sarcomeric properties likely contribute differently to systolic vs. diastolic global LV dysfunction after MI.
Dual-phase contrast-enhancement multislice computed tomography imaging for the assessment of elderly patients with acute myocardial infarction after primary percutaneous coronary intervention

Shaofeng Guan,Weiyi Fang,Xinkai Qu,Jianding Ye,Yan Shen,Jing Jiao,

老年心脏病学杂志(英文版) , 2009,
Abstract: Background Evaluation of acute myocardial infarction after reperfusion by dual phase contrast-enhancement multislice computed tomography (MSCT) was implicated in porcine model. There have been few attempts to use this diagnostic modality for the early assessment of coronary reperfusion in patients with ST-elevation myocardial infarction (STEMI), especially after primary percutaneous coronary intervention (PCI). In elderly patients with STEMI, the safety issues remain unknown. Methods Dual phase contrast-enhancement MSCT examinations were performed in 11 elderly patients (≥60 years old) with STEMI within one week after primary PCI. The presence, location and enhancement pattern on MSCT were evaluated. MSCT findings were compared with the catheter angiographic results and area under the curve of creatine kinase (CK) release. Serum creatinine level was recorded before and after MSCT scan. Results MSCT scans were successfully performed in all the patients. Early myocardial perfusion defect (early defect, ED) was detected in all of the 11 patients (100%) in the early phase of the contrast bolus (subendocardial ED in 10 patients and transmural in 1 patient). Mean CT attenuation value of ED was significantly different from CT attenuation value of remote myocardium (46±17 HU vs 104 ± 17 HU; P < 0.01). Location of ED area correlated well with infarction related artery territory on catheter angiography in all of the 11 patients (100%). On delayed phase of MSCT scan, different enhancement patterns were observed: isolated subendocardial late enhancement (LE) in 6 patients, subendocardial residual perfusion defect (RD) and subepicardial LE in 1 patient, subendocardial RD in 4 patients. Infarct volume assessed by MSCT correlated well with area under the curve CK release (R=0.72, P < 0.01). Serum creatinine level after MSCT scan showed no difference with that before MSCT scan. Conclusion Dual phase MSCT could be safely implicated in elderly patients with STEMI. Variable abnormal myocardial enhancement patterns were seen on dual phase MSCT in these patients with STEMI after primary PCI. Assessment of myocardial attenuation on MSCT gives additional information of the location and extent of infarction after reperfusion.
Smad3 Inactivation and MiR-29b Upregulation Mediate the Effect of Carvedilol on Attenuating the Acute Myocardium Infarction-Induced Myocardial Fibrosis in Rat  [PDF]
Jie-Ning Zhu, Ren Chen, Yong-Heng Fu, Qiu-Xiong Lin, Shuai Huang, Lin-Lin Guo, Meng-Zhen Zhang, Chun-Yu Deng, Xiao Zou, Shi-Long Zhong, Min Yang, Jian Zhuang, Xi-Yong Yu, Zhi-Xin Shan
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0075557
Abstract: Carvedilol, a nonselective β-adrenoreceptor antagonist, protects against myocardial injury induced by acute myocardium infarction (AMI). The mechanisms underlying the anti-fibrotic effects of carvedilol are unknown. Recent studies have revealed the critical role of microRNAs (miRNAs) in a variety of cardiovascular diseases. This study investigated whether miR-29b is involved in the cardioprotective effect of carvedilol against AMI-induced myocardial fibrosis. Male SD rats were randomized into several groups: the sham surgery control, left anterior descending (LAD)?surgery-AMI model, AMI plus low-dose carvedilol treatment (1 mg/kg per day, CAR-L), AMI plus medium-dose carvedilol treatment (5 mg/kg per day, CAR-M) and AMI plus high-dose carvedilol treatment (10 mg/kg per day, CAR-H). Cardiac remodeling and impaired heart function were observed 4 weeks after LAD surgery treatment; the observed cardiac remodeling, decreased ejection fraction, and fractional shortening were rescued in the CAR-M and CAR-H groups. The upregulated expression of Col1a1, Col3a1, and α-SMA mRNA was significantly reduced in the CAR-M and CAR-H groups. Moreover, the downregulated miR-29b was elevated in the CAR-M and CAR-H groups. The?in vitro?study showed that Col1a1, Col3a1, and α-SMA were downregulated and miR-29b was upregulated by carvedilol in a dose-dependent manner in rat cardiac fibroblasts. Inhibition of ROS-induced Smad3 activation by carvedilol resulted in downregulation of Col1a1, Col3a1, and α-SMA and upregulation of miR-29b derived from the miR-29b-2 precursor. Enforced expression of miR-29b significantly suppressed Col1a1, Col3a1, and α-SMA expression. Taken together, we found that smad3 inactivation and miR-29b upregulation contributed to the cardioprotective activity of carvedilol against AMI-induced myocardial fibrosis.
Lipopolysaccharide preconditioning enhances the efficacy of mesenchymal stem cells transplantation in a rat model of acute myocardial infarction
Yongwei Yao, Fumin Zhang, Liansheng Wang, Guohui Zhang, Zhaojun Wang, Jianmei Chen, Xiang Gao
Journal of Biomedical Science , 2009, DOI: 10.1186/1423-0127-16-74
Abstract: Acute myocardial infarction model was developed by left anterior descending coronary artery ligation. 60 rats were divided into 4 groups randomly and given an intramyocardial injection of one of the following treatments: 30 μl PBS (control group), 3 × 106 wild MSCs/30 μl (wMSCs group), 3 × 106 LPS-preconditioned wild MSCs/30 μl (LPS-wMSCs group), or 3 × 106 LPS-preconditioned TLR4 gene deleted MSCs/30 μl (LPS-tMSCs group). After 3 weeks, LPS-preconditioned wild MSCs transplantation ameliorated cardiac function and reduced fibrosis of infarcted myocardium. Vascular density was markedly increased in LPS-wMSCs group compared with other three groups. Survival rate of engrafted MSCs was elevated and apoptosis of myocardium was reduced in infarcted heart. Expression of vascular endothelial growth factor (VEGF) and phospho-Akt was increased in the infarcted myocardium after transplantation of LPS-preconditioned MSCs.LPS preconditioning enhanced survival of engrafted MSCs, stimulated expression of VEGF and activated PI3K/Akt pathway. LPS preconditioning before MSCs transplantation resulted in superior therapeutic neovascularization and recovery of cardiac function. LPS preconditioning provided a novel strategy in maximizing biologic and functional properties of MSCs.Despite the clinical success of reperfusion therapy, a large proportion of patients develop myocardial necrosis, ventricular remodelling and resultant congestive heart failure after acute myocardial infarction (AMI) [1]. Mesenchymal stem cells (MSCs)-based regenerative therapy is currently regarded as an alternative approach to salvage the MI hearts [2-4]. However, a major challenge to MSCs therapy is that transplanted cells undergo apoptosis, as they are exposed to an extremely harsh microenvironment in the infarcted heart. The efficiency of MSCs transplantation is limited by lower survival rate of MSCs [5,6]. Therefore, protection of MSCs against apoptosis is critical for successful cellular therapy. Novel str
MultiContrast Delayed Enhancement (MCODE) improves detection of subendocardial myocardial infarction by late gadolinium enhancement cardiovascular magnetic resonance: a clinical validation study  [cached]
Bandettini W Patricia,Kellman Peter,Mancini Christine,Booker Oscar
Journal of Cardiovascular Magnetic Resonance , 2012, DOI: 10.1186/1532-429x-14-83
Abstract: Background Myocardial infarction (MI) documented by late gadolinium enhancement (LGE) has clinical and prognostic importance, but its detection is sometimes compromised by poor contrast between blood and MI. MultiContrast Delayed Enhancement (MCODE) is a technique that helps discriminate subendocardial MI from blood pool by simultaneously providing a T2-weighted image with a PSIR (phase sensitive inversion recovery) LGE image. In this clinical validation study, our goal was to prospectively compare standard LGE imaging to MCODE in the detection of MI. Methods Imaging was performed on a 1.5 T scanner on patients referred for CMR including a LGE study. Prospective comparisons between MCODE and standard PSIR LGE imaging were done by targeted, repeat imaging of slice locations. Clinical data were used to determine MI status. Images at each of multiple time points were read on separate days and categorized as to whether or not MI was present and whether an infarction was transmural or subendocardial. The extent of infarction was scored on a sector-by-sector basis. Results Seventy-three patients were imaged with the specified protocol. The majority were referred for vasodilator perfusion exams and viability assessment (37 ischemia assessment, 12 acute MI, 10 chronic MI, 12 other diagnoses). Forty-six patients had a final diagnosis of MI (30 subendocardial and 16 transmural). MCODE had similar specificity compared to LGE at all time points but demonstrated better sensitivity compared to LGE performed early and immediately before and after the MCODE (p = 0.008 and 0.02 respectively). Conventional LGE only missed cases of subendocardial MI. Both LGE and MCODE identified all transmural MI. Based on clinical determination of MI, MCODE had three false positive MI’s; LGE had two false positive MI’s including two of the three MCODE false positives. On a per sector basis, MCODE identified more infarcted sectors compared to LGE performed immediately prior to MCODE (p < 0.001). Conclusion While both PSIR LGE and MCODE were good in identifying MI, MCODE demonstrated more subendocardial MI’s than LGE and identified a larger number of infarcted sectors. The simultaneous acquisition of T1 and T2-weighted images improved differentiation of blood pool from enhanced subendocardial MI.
Cardiovascular magnetic resonance of the myocardium at risk in acute reperfused myocardial infarction: comparison of T2-weighted imaging versus the circumferential endocardial extent of late gadolinium enhancement with transmural projection
Joey FA Ubachs, Henrik Engblom, David Erlinge, Stefan Jovinge, Erik Hedstr?m, Marcus Carlsson, H?kan Arheden
Journal of Cardiovascular Magnetic Resonance , 2010, DOI: 10.1186/1532-429x-12-18
Abstract: Thirty-seven patients with early reperfused first-time ST-segment elevation myocardial infarction underwent CMR imaging within the first week after percutaneous coronary intervention. The ability of endocardial extent of infarction by LGE CMR to assess MaR was evaluated using T2-weighted imaging as the reference method.MaR determined with T2-weighted imaging (34 ± 10%) was significantly higher (p < 0.001) compared to the MaR determined with endocardial extent of infarction (23 ± 12%). There was a weak correlation between the two methods (r2 = 0.17, p = 0.002) with a bias of -11 ± 12%. Myocardial salvage determined with T2-weighted imaging (58 ± 22%) was significantly higher (p < 0.001) compared to myocardial salvage determined with endocardial extent of infarction (45 ± 23%). No MaR could be determined by endocardial extent of infarction in two patients with aborted myocardial infarction.This study demonstrated that the endocardial extent of infarction as assessed by LGE CMR underestimates MaR in comparison to T2-weighted imaging, especially in patients with early reperfusion and aborted myocardial infarction.The myocardium at risk (MaR), defined as the hypoperfused myocardium during acute coronary occlusion will be subject to infarction if no reperfusion occurs[1]. The ability to assess MaR in relation to the final infarct size enables determination of myocardial salvage and, consequently, the efficacy of reperfusion therapy in patients with acute coronary occlusion [2,3].Currently, the most widely used method to determine myocardial perfusion defects is myocardial perfusion single photon emission computed tomography (SPECT). This technique can be used to assess MaR in the acute setting by intravenously injecting a perfusion tracer during coronary occlusion [4,5]. However, this approach has limitations in the clinical setting since the patient needs to have the perfusion tracer injected prior to reperfusion and undergo imaging in a gamma camera within approximately
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