Chronic Myocardial Infarction Research Articles

MiR-103 inhibiting cardiac hypertrophy through inactivation of myocardial cell autophagy via targeting TRPV3 channel in rat hearts.

Cardiac hypertrophy is a common pathological change frequently accompanied by chronic hypertension and myocardial infarction. Nevertheless, the pathophysiological mechanisms of cardiac hypertrophy have never been elucidated. Recent studies indicated that miR‐103 expression was significantly decreased in heart failure patients. However, less is known about the role of miR‐103 in cardiac hypertrophy. The present study was designed to investigate the relationship between miR‐103 and the mechanism of pressure overload‐induced cardiac hypertrophy. TRPV3 protein, cardiac hypertrophy marker proteins (BNP and β‐MHC) and autophagy associated proteins (Beclin‐1 and LC3‐II) were up‐regulated, as well as, miR‐103 expression and autophagy associated proteins (p62) were down‐regulated in cardiac hypertrophy models in vivo and in vitro respectively. Further results indicated that silencing TRPV3 or forcing overexpression of miR‐103 could dramatically inhibit cell surface area, relative fluorescence intensity of Ca2+ signal and the expressions of BNP, β‐MHC, Beclin‐1 and LC3‐II, but promote p62 expression. Moreover, TRPV3 protein was decreased in neonatal rat ventricular myocyte transfected with miR‐103, but increased by AMO‐103. Co‐transfection of the miR‐103 with the luciferase reporter vector into HEK293 cells caused a sharp decrease in luciferase activity compared with transfection of the luciferase vector alone. The miR‐103‐induced depression of luciferase activity was rescued by an AMO‐103. These findings suggested that TRPV3 was a direct target of miR‐103. In conclusion, miR‐103 could attenuate cardiomyocyte hypertrophy partly by reducing cardiac autophagy activity through the targeted inhibition of TRPV3 signalling in the pressure‐overloaded rat hearts.

Results of Coronary Artery Bypass Graft Surgery in Sharq Elmadina Hospital, Alexandria

Background: coronary artery bypass graft (CABG) surgery has been shown to be an effective method for treating angina pectoris and prolonging life in patients with severe coronary artery disease. Aim of the Work: to assess postoperative short-term results of coronary artery bypass graft surgery in Shark Elmedina hospital, Alexandria. Patients and Methods: This retrospective study was conducted on 170 patients with isolated ischemic heart disease admitted to Shark Elmadina hospital from January 2016 to January 2017. In the current study, pre-operative data were collected to identify the risk factors that may affect the outcome of surgery and intraoperative data and post-operative complications. Results: The most common risk factors were dyslipidemia (64.7%), hypertension (57.1%), diabetes mellitus which represents 50%, smoking which represents 37,6%, peripheral vascular disease which represents 31,7%. Other risk factors which had a low percent were history of chronic hepatic disease, previous stroke or myocardial infarction or lung disease or renal disease. What is worth to mention that echo preoperative affects the outcome of surgery as in our study EF of patients’ ranges from 40% to 75%. Intraoperative data also affects the outcome of surgery as number of grafts as there was one patient had done 5 grafts and 34 patients have done 4 grafts. Another important event was LLIMA dissection as there were 9 patients have dissected LIMA during harvesting. Another event was endartrectomy as there were 11 patients have LAD endartrectomy, 6 patients have RCA endartrectomy. Long bypass time and clamp time affects the results of surgery maximum bypass time 200 minute and maximum clamp time 120 minute. Post-operative ICU and ward stay affects the results as maximum ICU or ward stay was 9 days. The most common complication was wound infection which had an incidence 7% and the second complication was renal impairment which had an incidence 5.2%, reopening (2.9%), elevated liver enzymes which represents 2,3% and other complications which had low incidence as pleural effusion, lung atelectasis and stoke. Finally, mortality was 1.1%. Conclusion: CABG surgery is safe and the risk of major complications is low. Although major complications occur rarely they pose a great challenge to the patient and the surgeon. Early recognition and management of major complications are paramount to long term outcome.

Improved co-registration of ex-vivo and in-vivo cardiovascular magnetic resonance images using heart-specific flexible 3D printed acrylic scaffold combined with non-rigid registration

BackgroundEx-vivo cardiovascular magnetic resonance (CMR) imaging has played an important role in the validation of in-vivo CMR characterization of pathological processes. However, comparison between in-vivo and ex-vivo imaging remains challenging due to shape changes occurring between the two states, which may be non-uniform across the diseased heart. A novel two-step process to facilitate registration between ex-vivo and in-vivo CMR was developed and evaluated in a porcine model of chronic myocardial infarction (MI).MethodsSeven weeks after ischemia-reperfusion MI, 12 swine underwent in-vivo CMR imaging with late gadolinium enhancement followed by ex-vivo CMR 1 week later. Five animals comprised the control group, in which ex-vivo imaging was undertaken without any support in the LV cavity, 7 animals comprised the experimental group, in which a two-step registration optimization process was undertaken. The first step involved a heart specific flexible 3D printed scaffold generated from in-vivo CMR, which was used to maintain left ventricular (LV) shape during ex-vivo imaging. In the second step, a non-rigid co-registration algorithm was applied to align in-vivo and ex-vivo data. Tissue dimension changes between in-vivo and ex-vivo imaging were compared between the experimental and control group. In the experimental group, tissue compartment volumes and thickness were compared between in-vivo and ex-vivo data before and after non-rigid registration. The effectiveness of the alignment was assessed quantitatively using the DICE similarity coefficient.ResultsLV cavity volume changed more in the control group (ratio of cavity volume between ex-vivo and in-vivo imaging in control and experimental group 0.14 vs 0.56, p < 0.0001) and there was a significantly greater change in the short axis dimensions in the control group (ratio of short axis dimensions in control and experimental group 0.38 vs 0.79, p < 0.001). In the experimental group, prior to non-rigid co-registration the LV cavity contracted isotropically in the ex-vivo condition by less than 20% in each dimension. There was a significant proportional change in tissue thickness in the healthy myocardium (change = 29 ± 21%), but not in dense scar (change = − 2 ± 2%, p = 0.034). Following the non-rigid co-registration step of the process, the DICE similarity coefficients for the myocardium, LV cavity and scar were 0.93 (±0.02), 0.89 (±0.01) and 0.77 (±0.07) respectively and the myocardial tissue and LV cavity volumes had a ratio of 1.03 and 1.00 respectively.ConclusionsThe pattern of the morphological changes seen between the in-vivo and the ex-vivo LV differs between scar and healthy myocardium. A 3D printed flexible scaffold based on the in-vivo shape of the LV cavity is an effective strategy to minimize morphological changes in the ex-vivo LV. The subsequent non-rigid registration step further improved the co-registration and local comparison between in-vivo and ex-vivo data.

The unique mechanism of functional mitral regurgitation in acute myocardial infarction: a prospective dynamic 4D quantitative echocardiographic study.

Mechanisms of chronic ischaemic mitral regurgitation (IMR) are well-characterized by apically tethered leaflet caused by papillary muscles (PMs) displacement and adynamic mitral apparatus. We investigated the unique geometry and dynamics of the mitral apparatus in first acute myocardial infarction (MI) by using quantified 3D echocardiography. We prospectively performed 3D echocardiography 2.3 ± 1.8 days after first MI, in 174 matched patients with (n = 87) and without IMR (n = 87). 3D echocardiography of left ventricular (LV) volumes and of mitral apparatus dynamics throughout cardiac cycle was quantified. Similar mitral quantification was obtained at chronic post-MI stage (n = 44). Mechanistically, acute IMR was associated with larger and flatter annulus (area 9.29 ± 1.74 cm2 vs. 8.57 ± 1.94 cm2, P = 0.002, saddle shape 12.7 ± 4.5% vs. 15.0 ± 4.6%, P = 0.001), and larger tenting (length 6.36 ± 1.78 mm vs. 5.60 ± 1.55 mm, P = 0.003) but vs. chronic MI, mitral apparatus displayed smaller alterations (all P < 0.01) and annular size, PM movement remained dynamic (all P < 0.01). Specific to acute IMR, without PM apical displacement (P > 0.70), greater separation (21.7 ± 4.9 mm vs. 20.0 ± 3.4 mm, P = 0.01), and widest angulation of PM (38.4 ± 6.2° for moderate vs. 33.5 ± 7.3° for mild vs. 31.4 ± 6.3° for no-IMR, P = 0.0009) wider vs. chronic MI (P < 0.01). 3D echocardiography of patients with first MI provides insights into unique 4D dynamics of the mitral apparatus in acute IMR. Mitral apparatus remained dynamic in acute MI and distinct IMR mechanism in acute MI is not PM displacement seen in chronic IMR but separation and excess angulation of PM deforming the mitral valve, probably because of sudden-onset regional wall motion abnormality without apparent global LV remodelling. This specific mechanism should be considered in novel therapeutic strategies for IMR complicating acute MI.

Determinants of Myocardial Strain in Experimental Chronic Myocardial Infarction

We evaluated the relationships between regional myocardial strain measured by speckle tracking echocardiography and viability, fibrosis, hypertrophy and oxygen consumption in the infarcted or remote myocardium in a pig model of chronic myocardial infarction (MI). Thirteen farm pigs with surgical occlusion of the left anterior descending coronary artery and five sham-operated pigs were studied 3 mo post-MI. Computed tomography revealed significant left ventricle remodeling. Reduced radial or circumferential strain identified areas of transmural infarction (area under the curve: 0.82 and 0.79, respectively). In the remote non-infarcted area, radial strain correlated inversely with the amount of fibrosis (r = –0.66, p = 0.04) and myocyte hypertrophy (r = –0.68, p = 0.03). Radial strain rate inversely correlated with myocardial resting oxygen consumption assessed with 11C-labeled acetate positron emission tomography (r = –0.71, p = 0.006). In conclusion, myocardial strain and strain rate reflect fibrosis, hypertrophy and oxygen consumption of the remote areas after MI.

Characterization and implications of the dynamics of eosinophils in blood and in the infarcted myocardium after coronary reperfusion.

ObjectiveWe characterized the dynamics of eosinophils in blood and in the infarcted myocardium in patients and in a swine model of reperfused myocardial infarction (MI). The association of eosinophil dynamics with various outcomes was assessed.MethodsSerial eosinophil count and pre-discharge cardiac magnetic resonance were carried out in a prospective series of 620 patients with a first ST-elevation MI. In a swine model of reperfused MI, the dynamics of circulating eosinophils and their presence in the infarcted myocardium were determined. In autopsies from chronic MI patients, eosinophils were quantified.ResultsPatient eosinophil count sharply decreased 12h post-reperfusion compared to arrival. A lower minimum eosinophil count was associated with more extensive edema, microvascular obstruction, and infarct size as measured by cardiac magnetic resonance, and also with a higher rate of cardiac events (death, re-infarction, or heart failure) during follow-up. In the experimental model, eosinophil count boosted during ischemia and dropped back immediately post-reperfusion. Myocardial samples revealed progressive eosinophil migration into the infarcted myocardium, especially areas with microvascular obstruction. Markers of eosinophil maturation and survival (interleukin-5), degranulation (eosinophil cationic protein) and migration (eotoxin-1) were detected in the blood of patients, and in porcine myocardium. Eosinophil infiltration was detected in autopsies from chronic MI patients.ConclusionEosinopenia post-MI was associated with an impaired cardiac structure and adverse events. The decay in circulating eosinophils soon after reperfusion mirrors their migration into the infarcted myocardium, as reflected by their presence in heart samples from swine and patients. Further studies are needed to understanding this unexplored pathway and its therapeutic implications.

Adding Speckle-Tracking Echocardiography to Visual Assessment of Systolic Wall Motion Abnormalities Improves the Detection of Myocardial Infarction

The aim of this study was to investigate whether speckle-tracking echocardiography (STE) improves the detection of myocardial infarction (MI) over visual assessment of systolic wall motion abnormalities (SWMAs) using delayed enhancement cardiac magnetic resonance imaging as a reference. Transthoracic echocardiography was performed in 95 patients with first ST segment elevation MI 110days (interquartile range, 97-171days) after MI and in 48 healthy control subjects. Two experienced observers independently assessed SWMAs. Separately, longitudinal peak negative, peak systolic, end-systolic, global strain, and strain rate were measured and averaged for the American Heart Association-recommended coronary artery perfusion territories. Receiver operating characteristic analysis was used to determine a single optimal cutoff value for each strain parameter. The diagnostic accuracy of an algorithm combining visual assessment and STE was evaluated. Median infarct size and transmurality were 15% (interquartile range, 7%-24%) and 64% (interquartile range, 46%-78%), respectively. Sensitivity, specificity, and accuracy of visual assessment to detect MI were 74% (95% CI, 63%-82%), 85% (95% CI, 72%-93%), and 78% (95% CI, 70%-84%), respectively. Among the strain parameters, SR had the highest diagnostic accuracy (area under the curve, 0.88; 95% CI, 0.83-0.94; cutoff value, -0.97sec-1). The combination with STE improved sensitivity compared with visual assessment alone (94%; 95% CI, 86%-97%; P<.001), minimally affecting specificity (79%; 95% CI, 65%-89%; P=.607). Overall accuracy improved to 89% (95% CI, 82%-93%; P=.011). Multivariate analysis accounting for age and sex demonstrated that SR was independently associated with MI (odds ratio, 2.0; 95% CI, 1.6-2.7). The sensitivity and diagnostic accuracy of visually detecting chronic MI by assessing SWMAs are moderate but substantially improve when adding STE.

Myocardial Partition Coefficient of Gadolinium: A Pilot Study in Patients With Acute Myocarditis, Chronic Myocardial Infarction, and in Healthy Volunteers

BackgroundThe tissue-blood partition coefficient (PC) of gadolinium, derived from T1 measurements, reflects myocardial connective tissue fraction and tissue injury, increasing in proportion with edema or fibrosis. We determined the myocardial PC of gadolinium in patients with acute myocarditis, chronic myocardial infarction (MI), and healthy volunteers. We hypothesized that the characteristics of the injured myocardium in patients with MI and myocarditis may differ and that the PC will be higher in chronically injured myocardium (MI) compared with acutely injured myocardium (myocarditis). MethodsWe performed late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging and T1 mapping before and after administration of gadolinium (0.1 mmol/kg Gd-BOPTA) at 3 Tesla in 10 healthy volunteers (47.1 ± 12.4 years), 18 patients with chronic MI (62.5 ± 8.1 years), and 16 patients with acute myocarditis (42.5 ± 13.9 years). ResultsIn patients with chronic MI and focal scar by LGE, the whole left ventricular myocardial PC (0.45 ± 0.05) was higher compared with patients with MI without focal scar (0.39 ± 0.03, P = 0.02) but not significantly different from whole myocardial PC in volunteers (0.40 ± 0.05) or patients with myocarditis (0.41 ± 0.05). The PC in myocarditis scars was lower than in chronic MI scars (0.60 ± 0.12 vs 0.77 ± 0.16, P = 0.016). The relationships of PC and scar burden, expressed as % LGE, were similar and significant for the 2 groups (P = 0.042). ConclusionThe tissue-blood partition coefficient of Gd-BOPTA is elevated in areas of acute and chronic myocardial injury and may serve as a marker for disease activity and density of scars, which was found to be higher in chronic MI than in acute myocarditis.

Incidence of left ventricular thrombus formation in acute and chronic anteroseptal myocardial infarction

Incidence of left ventricular thrombus formation in acute and chronic anteroseptal myocardial infarction

Shensong Yangxin capsule reduces atrial fibrillation susceptibility by inhibiting atrial fibrosis in rats with post-myocardial infarction heart failure

PurposeShensong Yangxin (SSYX) capsule is a traditional Chinese medicine that has been used widely to treat cardiac arrhythmia. This study aimed to assess whether SSYX prevents atrial fibrillation (AF) after chronic myocardial infarction (MI)-induced heart failure and to determine the underlying mechanisms.Materials and methodsThe study included 45 male Sprague Dawley rats. The rats underwent MI induction or sham surgery. One week after MI induction surgery, we performed serial echocardiography and administered SSYX capsule to some rats that experienced MI. After 4 weeks of treatment, AF inducibility was assessed with transesophageal programmed electrical stimulation technology. Additionally, multielectrode array assessment, histological analysis, and Western blot analysis were performed.ResultsAF inducibility was significantly lower in SSYX rats than in MI rats (33.3% vs 73.3%, P<0.05). Additionally, conduction velocities in the left atrium were greater in SSYX rats than in MI rats. Moreover, SSYX decreased left atrial fibrosis, downregulated TGF-β1, MMP-9, TIMP-I, and type I and III collagen expressions, and inhibited the differentiation of cardiac fibroblasts to myofibroblasts.ConclusionSSYX reduces AF inducibility after MI by improving left atrial conduction function via the inhibition of left atrial fibrosis. It prevents the development of an MI-induced vulnerable substrate for AF.

Chronic Disease Population Risk Tool (CDPoRT): a study protocol for a prediction model that assesses population-based chronic disease incidence

BackgroundPopulation-based risk prediction tools exist for individual chronic diseases. From a population health perspective, studying chronic diseases together provides a comprehensive view of the burden of disease in the population. Thus, public health officials and health policymakers would benefit from a prediction tool that measures the incidence of chronic diseases compositely. This study protocol proposes the development and validation of the Chronic Disease Population Risk Tool (CDPoRT) that will predict the incidence of six chronic diseases in the population setting using multivariable modeling techniques.MethodsCDPoRT will be built using population-based responses to the first six cycles of the Canadian Community Health Survey linked to health administrative data in Ontario and Manitoba from 2000 to 2014. Predictors including modifiable lifestyle risk factors (i.e., alcohol consumption, cigarette smoking, diet, and physical activity) will be used to predict time-to-chronic disease incidence (i.e., congestive heart failure, chronic obstructive pulmonary disease, diabetes, lung cancer, myocardial infarction, and stroke including transient ischemic heart attack). Sex-specific Royston-Parmar models will be used for model development and validation with death free of chronic disease as a competing risk. CDPoRT will be developed using an Ontario derivation cohort consisting of 47,960 females and 38,267 males with 7035 and 6220 chronic disease events, respectively. The model will be validated using split-sample validation using an Ontario validation cohort consisting of 20,325 females and 16,627 males with 2972 and 2658 chronic disease events, respectively. The model will be externally validated in the Manitoba validation cohort (i.e., geographic validation) expected to consist of 11,800 females and 9700 males with 1650 and 1550 chronic disease events, respectively. Measures of overall predictive accuracy (e.g., Nagelkerke’s R2), discrimination (e.g., Harrell’s concordance statistic), and calibration (e.g., calibration plots) will be used to assess predictive performance.DiscussionTo the extent of our knowledge, CDPoRT will be the first population-based regression prediction model that will predict the incidence of multiple chronic diseases simultaneously at the population level.

Osteoprotegerin and Myocardial Fibrosis in Patients with Aortic Stenosis

Left ventricular myocardial fibrosis in patients with aortic stenosis (AS) confers worse prognosis. Plasma osteoprotegerin (OPG), a cytokine from the TNF receptor family, correlates with the degree of valve calcification in AS, reflecting the activity of the tissue RANKL/RANK/OPG (receptor activator of nuclear factor κΒ ligand/RANK/osteoprotegerin) axis, and is associated with poorer outcomes in AS. Its association with myocardial fibrosis is unknown. We hypothesised that OPG levels would reflect the extent of myocardial fibrosis in AS. We included 110 consecutive patients with AS who had undergone late-gadolinium contrast enhanced cardiovascular magnetic resonance (LGE-CMR). Patients were characterised according to pattern of fibrosis (no fibrosis, midwall fibrosis, or chronic myocardial infarction fibrosis). Serum OPG was measured with ELISA and compared between groups defined by valve stenosis severity. Some 36 patients had no fibrosis, 38 had midwall fibrosis, and 36 had chronic infarction. Patients with midwall fibrosis did not have higher levels of OPG compared to those without fibrosis (6.78 vs. 5.25 pmol/L, p = 0.12). There was no difference between those with midwall or chronic myocardial infarction fibrosis (6.78 vs. 6.97 pmol/L, p = 0.27). However, OPG levels in patients with chronic myocardial infarction fibrosis were significantly higher than those without fibrosis (p = 0.005).

Primary Effect of SERCA 2a Gene Transfer on Conduction Reserve in Chronic Myocardial Infarction.

Background SERCA2a gene transfer (GT) improves mechano‐electrical function in animal models of nonischemic heart failure Whether SERCA2a GT reverses pre‐established remodeling at an advanced stage of ischemic heart failure is unclear. We sought to uncover the electrophysiological effects of adeno‐associated virus serotype 1.SERCA2a GT following myocardial infarction (MI).Methods and ResultsPigs developed mechanical dysfunction 1 month after anterior MI, at which point they received intracoronary adeno‐associated virus serotype 1.SERCA2a (MI+SERCA2a) or saline (MI) and were maintained for 2 months. Age‐matched naive pigs served as controls (Control). In vivo ECG‐and‐hemodynamic properties were assessed before and after dobutamine stress. The electrophysiological substrate was measured using optical action potential (AP) mapping in controls, MI, and MI+SERCA2a preparations. In vivo ECG measurements revealed comparable QT durations between groups. In contrast, prolonged QRS duration and increased frequency of R′ waves were present in MI but not MI+SERCA2a pigs relative to controls. SERCA2a GT reduced in in vivo arrhythmias in response to dobutamine. Ex vivo preparations from MI but not MI+SERCA2a or control pigs were prone to pacing‐induced ventricular tachycardia and fibrillation. Underlying these arrhythmias was pronounced conduction velocity slowing in MI versus MI+SERCA2a at elevated rates leading to ventricular tachycardia and fibrillation. Reduced susceptibility to ventricular tachycardia and fibrillation in MI+SERCA2a pigs was not related to hemodynamic function, contractile reserve, fibrosis, or the expression of Cx43 and Nav1.5. Rather, SERCA2a GT decreased phosphoactive CAMKII‐delta levels by >50%, leading to improved excitability at fast rates.Conclusions SERCA2a GT increases conduction velocity reserve, likely by preventing CAMKII overactivation. Our findings suggest a primary effect of SERCA2a GT on myocardial excitability, independent of altered mechanical function.

Biochemical effect of curcumin on experimentally induced myocardial injury in rats

Myocardial infarction (MI) is one of the main causes of death from cardiovascular disease. Curcumin was shown to exert potent antioxidant, anti-inflammatory, antiangiogenic, antimutagenic, anticoagulant and antidiabetic activities. This study was done to investigate the protective effects of curcumin in isoproterenol (ISO) induced myocardial injury in rats. Forty-eight rats were divided into 6 equal groups. Group I: (normal control) rats received no drugs. Group II :(curcumin) rats received curcumin (200 mg/kg b.wt/day) orally for 30 days. Group III: (acute myocardial infarction) rats injected ISO (20mg/kg b.wt /intraperitoneally) twice at the 29th and 30th days of experiment. Group IV: (chronic myocardial infarction) rats injected ISO (20mg/kg b.wt /intraperitoneally) twice at the 1st and 2nd days of experiment. Group V: (acute myocardial infarction + curcumin) rats received curcumin (200 mg/kg b.wt/day) for 30 days, then ISO was injected twice, at an interval of 24 hours, on the 29th and 30th days .Group VI: (chronic myocardial infarction + curcumin) rats injected ISO at the 1st and 2nd days of experiment and treated with curcumin for 30 days. Blood samples and heart tissue specimens were collected at the end of experimental period (30 days) for determination of serum Creatine kinase MB (CK-MB), Lactate dehydrogenase (LDH), cardiac Troponins (cTn) and Interleukin-1β (IL-1β). Moreover, heart tissues catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and L-Malondialdhyde (L-MDA) were also determined. The obtained results showed a significant increase in serum cardiac marker enzymes (CK-MB and LDH) activities, cTn and IL-1β concentrations in addition to L-MDA in heart tissues of ISO-induced myocardial injury in rats. However, GPx and CAT activities and GSH concentration in heart tissues of myocardial infarction induced in rats were markedly decreased. Curcumin treatment was able to protect rat myocardium against isoproternol induced myocardial ischemic damage and the protective effect was attributed to its antioxidant properties by inhibiting free radical generation.

Correlations of T2* Mapping with Delayed Gadolinium Enhancement in Chronic Myocardial Infarction Magnetic Resonance Imaging

Background: Scar tissue formation is a common phenomenon in myocardial infarctions. Contrast-enhanced cardiac magnetic resonance imaging is the modality of choice to evaluate the location and size of the scar tissue. Nevertheless, in patients with severe kidney impairment, administration of gadolinium is contraindicated. Objectives: So the aim of this study was to substitute a safe way for myocardial infarction assessments in patients with a history of renal function impairment. We assessed the T2* quantitative value changes in myocardial infarction-related scar tissue and compared them with normal/remote myocardial tissue T2* values to evaluate its application in non-contrast cardiac magnetic resonance imaging viability assessments. Patients and Methods: Twenty patients with a previous history of non ST-elevation myocardial infarction (NSTEMI) underwent cardiac magnetic resonance (CMR) examination with a 1.5T MR imaging scanner (Avanto, Siemens AG Healthcare Sector, Erlangen, Germany). The time interval between myocardial infarction occurrence and CMR assessment was at least six months. All the patients had normal kidney function. The imaging protocol consisted of three steps: the functional left-ventricular imaging; 8-echoes gradient recalled echo T2* mapping; and delayed/late gadolinium-enhancement imaging. The left-ventricle functional and T2* mapping assessments were done by CMR42 image analysis software (Circle Cardiovascular Imaging, Calgary, Canada). T2* values were calculated for 49 regions of interests (ROIs) at the infarction (14 ROIs), peri-infarction (12 ROIs), and remote/normal myocardial tissues (23 ROIs), and their means were compared statistically by the Leven’s test. Finally, the receiver operator characteristics curve was calculated. Results: T2* (mean ± SD) values of the normal/remote, peri-infarction, and infarcted myocardial tissues were calculated as 29.42 ± 4.50, 30.71 ± 4.86, and 35.46 ± 3.61, respectively. There was a significant alteration in the post-infarction scar tissue’s myocardial T2* values by comparison with the normal/remote myocardium (P 0.05). Area under the curve was 81% for patients evaluated for scars. Cutoff value of 31.70 yielded 92% sensitivity and 72% specificity. Conclusion: T2* relaxation time can provide useful and sensitive information on scar tissue formation location, and can offer a greater sensitivity into the non-contrast CMR imaging viability assessments besides other relaxation phenomena, especially the longitudinal relaxation time.

The prevalence of co-morbidities and their impact on physical activity in people with inflammatory rheumatic diseases compared with the general population: results from the UK Biobank.

ObjectivesTo compare the prevalence and incidence of chronic co-morbidities in people with inflammatory rheumatic and musculoskeletal diseases (iRMDs), and to determine whether the prevalent co-morbidities are associated with physical activity levels in people with iRMDs and in those without iRMDs.MethodsParticipants were recruited to the UK Biobank; a population-based cohort. Data were collected about demographics, physical activity, iRMDs (RA, PsA, AS, SLE) and other chronic conditions, including angina, myocardial infarction, stroke, hypertension, pulmonary disease, diabetes and depression. The standardized prevalence of co-morbidities in people with iRMDs was calculated. Cox regression was used to determine the relationship between the presence of an iRMD and an incident co-morbidity. The relationship between the presence (versus absence) of a (co-)morbidity and physical activity level (low, moderate, high) in people with iRMDs and in those without was assessed using multinomial logistic regression.ResultsA total of 488 991 participants were included. The estimated prevalence of each co-morbidity was increased in participants with an iRMD, compared with in those without, particularly for stroke in participants with SLE (standardized morbidity ratio (95% CI), 4.9 (3.6, 6.6). Compared with people with no iRMD and no morbidity, the odds ratios (95% CI) for moderate physical activity were decreased for: no iRMD and morbidity, 0.87 (0.85, 0.89); iRMD and no co-morbidity, 0.71 (0.64, 0.80); and iRMD and co-morbidity, 0.58 (0.54, 0.63).ConclusionHaving a (co-)morbidity is associated with reduced physical activity in the general population, and to a greater extent in participants with an iRMD. Optimal management of both iRMDs and co-morbidities may help to reduce their impact on physical activity.

Clinical Risk Factors for Postoperative Atrial Fibrillation among Patients after Cardiac Surgery.

Postoperative atrial fibrillation (POAF) is a common arrhythmia following cardiac surgery and is associated with increased health-care costs, complications, and mortality. The etiology of POAF is incompletely understood and its prediction remains suboptimal. Using data from published studies, we performed a systemic review and meta-analysis to identify preoperative clinical risk factors associated with patients at increased risk of POAF. A systematic search of PubMed, MEDLINE, and EMBASE databases was performed. Twenty-four studies that reported univariate analysis results regarding POAF risk factors, published from 2001 to May 2017, were included in this meta-analysis with a total number of 36,834 subjects. Eighteen studies were performed in the United States and Europe and 16 studies were prospective cohort studies. The standardized mean difference (SMD) between POAF and non-POAF groups was significantly different (reported as [SMD: 95% confidence interval, CI]) for age (0.55: 0.47-0.63), left atrial diameter (0.45: 0.15-0.75), and left ventricular ejection fraction (0.30: 0.14-0.47). The pooled odds ratios (ORs) (reported as [OR: 95% CI]) demonstrated that heart failure (1.56: 1.31-1.96), chronic obstructive pulmonary disease (1.36: 1.13-1.64), hypertension (1.29: 1.12-1.48), and myocardial infarction (1.18: 1.05-1.34) were significant predictors of POAF incidence, while diabetes was marginally significant (1.06: 1.00-1.13). The present analysis suggested that older age and history of heart failure were significant risk factors for POAF consistently whether the included studies were prospective or retrospective datasets.

Sustained release of basic fibroblast growth factor using gelatin hydrogel improved left ventricular function through the alteration of collagen subtype in a rat chronic myocardial infarction model.

Chronic myocardial infarction (CMI) tends to be resistant to treatments possibly due to extensive solid fibrotic scar, hypoxia mediated by poorly vascularized environment, and/or inflammation and apoptosis. Here we aimed to testify the therapeutic effects of sustained release of basic fibroblast growth factor (bFGF) using gelatin hydrogel (GH) in a rat chronic MI model and to elucidate the therapeutic mechanism including the alteration of extracellular matrix component. CMI model rats are prepared by the permanent ligation of proximal left anterior descending coronary artery. After 4weeks, GH sheets (GHSs) with bFGF (100µg) (bFGF group)or with phosphate-buffered saline (Vehicle group) were implanted to the CMI models to evaluate the effect of bFGF-GHS on chronic scar tissue. Sham operation group was also prepared (n = 5 for each). 4weeks after implantation, bFGF-GHS significantly improved cardiac contractile function (fractional shortening: 21.8 ± 1.1 vs 21.5 ± 1.3 vs 29.7 ± 1.8%; P < 0.001/fractional area change: 33.0 ± 1.4 vs 34.1 ± 2.3 vs 40.6 ± 1.8%; P < 0.001) (Sham vs Vehicle vs bFGF) accompanied with neovascularization. Immunohistochemical studies revealed that bFGF-GHS increased collagen III/I ratio indicating the alteration of solid scar tissue. Quantitative RT-PCR results showed a decrease of collagen I mRNA expression within border MI zone. The implantation of bFGF-GHS altered the collagen subtype of the fibrotic scar more suitable for tissue repair. The treatment of sustained-release bFGF may be promising for ischemic heart disease through chronic pathology.

Value of the Resting Electrocardiogram in Assessing Patients with Recent Onset Chest Pain A Study in Tertiary Care Hospital, Dhaka Bangladesh

Background: Chest pain or discomfort caused by acute coronary syndrome (ACS) or angina has a potentially poor prognosis, emphasizing the importance of prompt and accurate diagnosis. To evaluate a clinic set up specifically to assess patients with recent onset chest pain, particularly those presenting with a normal resting electrocargram.Method: The cross-sectional study was carried out from September 2016 to August 2017 in cardiology department of Shaheed Suhrawardy Medical College hospital, Sher-E-Bangla Nagar, Dhaka. Total 1000 consecutive patients with recent onset chest pain were evaluated within 24 hours of general practitioner referral, to find out the clinical diagnosis and management.Results: Total 1000 patients (535 men and 465women, mean age 51.5±11.4 years with range from 32 to 70 years) were assessed over 12 months. Most of the patients 844 (84.4%) had symptoms in duration of ≤30 days. Majority 433 (43.3%) patients had peptic ulcer disease (PUD), 317 (31.7%) patients had chronic stable angina (CSA), 94 (9.4%) had unstable angina (UA), 92 (9.2%) had anxiety neurosis (AN) and 64 (6.4%) had myocardial infarction (MI). Regarding outcome of the patients 525 (52.5%) [PUD: 433+ AN: 91] patients considered to have noncardiac pain and referred to medicine outpatient department (OPD) without further follow up. In a further 317 patients (31.7%, CSA) arrangements were made for outpatient review. Ninety four patients (9.4%, UA) were referred to National Institute of Cardiovascular diseases (NICVD) for admission out of them 61 patients were admitted for medical treatment &amp; 33 patients were discharged from emergency department whose troponin-I were negative. Remaining 64 (6.4%) acute MI patients were admitted into Coronary Care Unit (CCU) of NICVD, out of them 41 patients received streptokinase injection, 23 patients received Enoxaparin injection, after conservative treatment all patients were advised to do coronary angiography within 3 to 4 weeks. Among these 43 patients underwent coronary angiography within 4 weeks, 23 patients had coronary angioplasty, eleven patients had coronary bypass surgery and nine patients refused any intervention and discharged with medicine.Conclusion: This experience highlights the inadequacy of a routine electrocardiogram reporting service in patients with recent onset of chest pain. Clinical diagnosis found were peptic ulcer disease (PUD), chronic stable angina (CSA), unstable angina (UA), anxiety neurosis and myocardial infarction (MI). Regarding outcome of the patients were coronary angiography followed by coronary angioplasty, coronary artery bypass surgery, discharged with medicine and referred to out patients department of medicine unit.J Shaheed Suhrawardy Med Coll, December 2017, Vol.9(2); 65-68

Comparison of Angiogenic Activities of Three Neuropeptides, Substance P, Secretoneurin, and Neuropeptide Y Using Myocardial Infarction.

The interplay between neurogenesis and angiogenesis is crucial during the development mediated by neuro-angiogenic morphogens. In particular, the angiogenic activity of neuropeptides and their role in tissue regeneration have long been investigated for better understanding of their biological mechanisms and further applications. However, there have been few studies for direct comparison of angiogenic activities of neuropeptides for in vitro and in vivo models. In this study, we report that direct comparison of the angiogenic activities of neuropeptide Y, secretoneurin, and substance P (SP) immobilized on hydrogels in in vitro and in vivo experiments. A hyaluronic acid-based hydrogel is prepared by utilizing acrylated hyaluronic acid and thiolated peptides as a crosslinker and angiogenic factors, respectively. Angiogenic activities of three neuropeptides are evaluated not only by in vitro angiogenic and gene expression assays, but also by an in vivo chronic myocardial infarction model. The comparison of in vitro angiogenic activities of three peptides demonstrates that the SP-immobilized hydrogel shows a higher degree of cell network formation and angiogenic-specific genes than those of the other peptides and the control case. In addition, a three-dimensional angiogenic assay illustrates that more sprouting is observable in the SP group. Evaluation of regenerative activity in the chronic myocardial infarction model reveals that all three peptide-immobilized hydrogels induce increased cardiac function as well as structural regeneration. Among all the cases, the SP group provided the highest regenerative activity both in vitro and in vivo. In our comparison study, the SP-immobilized hydrogel shows the highest angiogenic activity and tissue regeneration among the test groups. This result suggests that nerve regeneration factors help angiogenesis in damaged tissues, which also highlights the importance of the neuro-angiogenic peptides as an element of tissue regeneration.