Myocardial Infarction

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MiRNAs as biomarkers of myocardial infarction: a meta-analysis.

MiRNAs as biomarkers of myocardial infarction: a meta-analysis.

Figure 4. The sensitivity, specificity, diagnostic OR, SROC curve with AUC and funnel plot for miR-1 levels of 7 studies in the diagnosis of myocardial infarction. (A) Sensitivity. (B) Specificity. (C) Diagnostic OR. (D) SROC curve with AUC. (E) Funnel plot. Df, degree of freedom; OR, odds ratio; SROC, summary receiver operator characteristics; AUC, area under the curve; SE, standard error; Q*, Q index. Balls, estimated respectively the sensitivity, specificity, diagnostic OR, AUC; Bars, 95% confidence intervals (CIs); Width of diamonds, pooled CIs. The size of each ball is proportional to the weight of each study in the meta-analysis. The SROC show all values of AUC and the area between the upper left and lower right curves represent the CIs of AUC for total miRNA levels. Values that cross the borders are not shown in these figures. Boxes in the funnel plot indicated the studies included in this meta- analysis.
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Protective Effects of Baicalin on Experimental Myocardial Infarction in Rats

Protective Effects of Baicalin on Experimental Myocardial Infarction in Rats

Methods: Fifty Sprague Dawley rats were randomly divided into the control, model, and low-, medium- and high-dose baicalin groups. The latter 3 groups were intraperitoneally injected with baicalin, with a dose of 12.5, 25 and 50 mg/ kg, respectively. Then, the myocardial infarction model was established. The hemodynamic of rats was tested, the serum lactate dehydrogenase (LDH), creatine kinase-MB (CK- MB), prostacyclin (PGI 2 ) and thromboxane A 2 (TXA 2 ) were

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Acute myocardial infarction in sub-Saharan Africa: the need for data.

Acute myocardial infarction in sub-Saharan Africa: the need for data.

Observational studies were included that reported the incidence or prevalence of AMI among any population within SSA. Published articles were required to be in English, Spanish, French or Portuguese, or have complete translations into one of those languages. The study definition of ‘‘acute myocardial infarction’’ was based on the universal definition of myocardial infarction, defined by a combination of clinical symptoms felt by the clinician to represent coronary ischemia within 24 hours of presentation to the hospital or during the present hospitalization and either EKG changes (new ST-segment elevation, new LBBB, new pathologic Q wave) or elevation of cardiac enzymes (troponin or CK-MB . 99th percentile) with or without ST-segment elevations on EKG.[12] Our study definition did not require biomarker elevations as most studies were conducted in areas without access to these tests. In situations where more than one study was conducted on the same data set, the study with more complete data was included. Studies were included from January 1992 through October 28, 2012.
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Genetic variations in circadian rhythm genes and susceptibility for myocardial infarction

Genetic variations in circadian rhythm genes and susceptibility for myocardial infarction

Human studies have identified genetic variants and expression patterns of circadian clock genes, such as ARNTL, CLOCK, CRY2, NPAS2 or PER2, that are associ- ated with metabolic syndrome, hypertension or diabetes mellitus type 2 (Ohkura et al., 2006; Scott, 2015). Circa- dian clock genes play a major role in hemostatic balance by regulating the fibrinolytic systems, and CLOCK and CRY genes are directly involved in this activity (Ohkura et al., 2006), and therefore increase the risk for CVD. A role of the circadian rhythm in cardiovascular function is firmly supported in all those studies, but our study found the con- nection of myocardial infarction and some of the circadian rhythm genes SNPs.
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Circulating NOS3 modulates left ventricular remodeling following reperfused myocardial infarction.

Circulating NOS3 modulates left ventricular remodeling following reperfused myocardial infarction.

In our setup, following myocardial ischemia biglycan, decorin and Timp1 mRNA levels are increased in BC−/EC+. It is tempting to speculate, that the levels are increased as a response to the augmented myocardial injury and, as a consequence, stabilize the collagen rich scar in this group. Biglycan and decorin are involved in the organisation of collagen fibril networks espe- cially collagen 1 and 3 [38, 39] and biglycan mRNA levels have been demonstrated to be in- creased in the infarcted zone after MI [40]. Biglycan deficiency leads to disturbed collagen deposition, disturbed remodeling and hemodynamic insufficiency after myocardial infarction with subsequent ventricular rupture [41, 42]. Furthermore, biglycan is known to protect cardi- omyocytes against hypoxia/ reoxygenation injury by activation of NOS3 [43]. In this context, the impact of biglycan on NOS3 in BC−/EC+ would be expected to be decreased due to missing circulating NOS3.
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Accuracy of Impedance Cardiography in Acute Myocardial Infarction: A Literature Review

Accuracy of Impedance Cardiography in Acute Myocardial Infarction: A Literature Review

The collection of data occurred in the period from January to August 2015. The following controlled descriptors were used to find the articles in databases: myocardial infarction, cardiography impedance, catheterization, Swan Ganz, invasive hemodynamic monitoring and hemodynamics. The composition of the sample met the inclusion criteria: Articles in Portuguese, English and Spanish; Articles that compared bioimpedance cardiography and invasive hemodynamic

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Histochemical and immunohistochemical analyses of the myocardial scar fallowing acute myocardial infarction

Histochemical and immunohistochemical analyses of the myocardial scar fallowing acute myocardial infarction

The human heart, just like the brain, is mostly com- posed of terminally differentiated cells, but it is not a termi- nally differentiated organ because it contains stem cells that can develop its regeneration 2, 3, 13, 23–27 . By the usage of Ki- 67 nuclear antigen, Beltrami et al. 8 has found out positive reaction associated with cell division in all nuclei of the large oval and elongated cells. Similar results were found in our research. These cells were negative to lymphocyte, leu- kocyte and endothelial markers. Ki-67 is a nuclear antigen and in our research it was positive in myocytes of an infarc- ted heart suggesting that cardimyocytes are divisional. By using alpha actin Beltrami et al. 8 have found in these cells its accumulation in the contractile ring what was also confirmed in our study. These results show that in the adult heart after experienced infarction, there is a myocyte subpopulation not terminally differentiated and capable to divide soon after in- farcton. In our research cells that were positive to Ki-67 nu- clear antigen were also positive to the usage of: PCNA, alpha actin, actin HHF35, myoglobin, myosin and desmin, but showed negative reaction to lymphocyte, leukocyte and en- dothelial markers. Other authors' 1, 5, 8 finding are the same suggesting possible myocyte regeneration after myocardial infarction 1, 2, 5, 8 . It has been proved that heart stem cells are capable to differentiate into three types of heart cells: car- diomyocytes, smooth muscle cells in the blood vessel wall and endothelial cells 12 . We have showed the presence of both smooth muscle and endothelial cells in the walls of the newly formed blood vessels in the scar after infarction. Stem cell factor can affect and activate all the three mentioned cells during myocardial ischemia and result in a significant increase in new myocyte formations 2, 12 . Myocardium regen- eration requires myocyte and blood vessels formation be- cause myocytes cannot live and grow without blood vessels. However, blood vessels formation alone will not regenerate the dead myocardium and its contractile activity after infarc- tion 7, 28, 29 . The preserved muscle fibers that we have found isolated in the myocardial scar after infarction were hyper- trophic with the large nucleus suggesting their participation in synchronous contractions of heart muscle and possibly in prevention of the heart aneurysm development.
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Current therapy of the right ventricle myocardial infarction

Current therapy of the right ventricle myocardial infarction

Background. Acute myocardial infarction of the right venricle (AMI-RV) is a separate subgroup within the scope of inferoposterior infarction of the left ventricle. It still rep- resents the population of patients at high risk due to numerous, often hardly predict- able complications and high mortality rate. Methods. In fifteen-year period (1987 − 2001) 3 765 patients with the acute myocardial infarction (AMI) of different lo- calizations of both sexes – 2 283 males and 1 482 females of the average age 61.4 ± 4.6 years were treated in our institution. Anterior myocardial infarction was di- agnosed in 2 146 (56.9%) patients, inferior in 1 619 (43.1%) patients, out of whom right ventricular infarction (RVI) was confirmed in 384 (23.7%). Thrombolytic therapy was administered in 163 (42.4%) patients with RVI, and in 53 (41.7%) of these pa- tients balloon dilatation was performed with coronary stent implantation in 24 (45.2%). Results. Favorable clinical effect of the combined thrombolytic therapy and percutaneous transluminal coronary angioplasty (PTCA) was achieved in 51 (96.1%), and in only 2 (3.9%) of patients the expected effect wasn't achieved. Myocardial revas- cularization was accomplished in 6 (3.6%) and 1 patient died. In 3 (3.4%) patients primary balloon dilatation with the implantation of intracoronary stent was performed within 6 hours from the onset of anginal pain. In the other group of 221 (57.5%) pa- tients with RVI who did not receive thrombolytic therapy, or it had no effect, 26 (11.7%) patients died, which indicated the validity and the efficacy of this treatment (p<0,01). In the whole group of patients with myocardial infarction of the right ventri- cle 31 (8.1%) died; in the group that received thrombolytic therapy and PTCA 5 (3.1%) died, while in the group treated in a conservative way 26 (11.7%) died. Con- clusion. Combined therapy was successful in the treatment of patients with RVI and should be administered whenever possible, since it was the best prevention of life- threatening complications and the decrease in the mortality of those patients.
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Prevalence and prognostic significance of silent myocardial ischemia in patients after myocardial infarction

Prevalence and prognostic significance of silent myocardial ischemia in patients after myocardial infarction

Background/Aim. Silent myocardial ischemia (MI) can be de- tected in subjects with any symptoms, in patients after myocardial in- farction and in coronary patients who have episodes of symptomatic, as well as of silent MI. This study was carried out to evaluate the fre- quency, characteristics and prognostic significance of silent MI de- tected in stress echocardiography test in patients after myocardial in- farction. Methods. In 210 patients within three months after myo- cardial infarction exercise test was performed. In those patients with ischemic ST depression on exercise electrocardiogram, in order to confirm MI stress echocardiography was additionally performed. To assess the incidence of major cariovascular events, all the patients were followed at least five years after the first myocardial infraction. Results. Out of 210 patients 88 (42%) had ischemic response during stress echocardiography test. Out of 88 patients with MI 54 (61%) had anginal pain (patients with symptomatic MI), while 34 (39%) were free of symptoms (patients with silent MI). Level of exercise test, heart rate, time to the onset of ST segment depression, and the magnitude of ST segment depression were similar in both subgroups of the patients with MI. Duration of exercise test was longer in pa- tients with silent MI (p < 0.05). Wall motion score index during stress echocardiography was higher in patients with symptomatic MI (p < 0.05). Coronary angiography findings were similar in patients with silent and those with symptomatic MI. During a five- years- follow-up period the occurrence of major cardic events (cardiac mortality and recurrent myocardial infarction) was similar in both subgroups of the patients with MI. Conclusion. In more than one third of patients after myocardial infarction silent MI during stress echocardiography was detected. The patients with silent ischemia had longer duration of exercise test and smaller wall motion score index on stress echocardiography. There was no difference in coro- nary angiography finding between patients with silent and those with symptomatic MI. The incidence of major cardiac events during a five- years- follow-up was similar in the patients with silent and those with symptomatic MI.
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Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation

Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation

Management of acute myocardial infarction in patients presenting with persistent.. ST-segment elevation # *.[r]

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Adjuvant antithrombotic therapy in ST-elevation myocardial infarction : a narrative review

Adjuvant antithrombotic therapy in ST-elevation myocardial infarction : a narrative review

1. Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC), Steg PG, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients present- ing with ST-segment elevation. Eur Heart J. 2012;33:2569---619. 2. Yanamala CM, Bundhun PK, Ahmed A. Comparing mortal- ity between fibrinolysis and primary percutaneous coronary intervention in patients with acute myocardial infarction: a systematic review and meta-analysis of 27 randomized- controlled trials including 11 429 patients. Coron Artery Dis. 2017;28:315---25.
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Assessing myocardial perfusion after myocardial infarction.

Assessing myocardial perfusion after myocardial infarction.

What Was the Subsequent Differential Diagnosis? Our patient presented with electrocardiogram changes of a myocardial infarction (MI). Although this is most likely due to coronary occlusion, the ST elevation may occur for reasons other than infarction (Box 1). Moreover, infarction need not result from coronary occlusion (Box 2). The electrocardiogram and echocardiogram thus both suggested a high probability of ischemia in the LAD territory. In order to stratify our patient’s prognosis, it would be important to determine whether the patient did indeed have the implied single vessel (LAD) coronary artery disease and whether the infarct territory was optimally revascularised at macro- and
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Diastolic Heart Function and Myocardial Electrical Instability in Patients with Q-wave Myocardial Infarction

Diastolic Heart Function and Myocardial Electrical Instability in Patients with Q-wave Myocardial Infarction

The treatment of acute MI was carried out in accordance with recommendations for the Management of Patients with ST-Elevation Myocardial Infarction and included thrombolytic therapy, early administration of beta-blockers, antiplatelet agents, anticoagulants, nitrates, statins, ACE inhibitors, and loop diuretics. All patients underwent clinical examination, including a physical examination, medical history, ECG in 12 conventional leads, echocardiography, and 24-hour ECG monitoring on the 10 th through the 14th days of MI.

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Medication adherence among persons with post-acute myocardial infarction

Medication adherence among persons with post-acute myocardial infarction

Financial status had a negative direct effect on medi- cation adherence. This means that even though most (78.1%) post-MI patients had low financial status (income < 5,000 baht/month), they were more likely to have a higher level of medication adherence because 71.6% were covered by Uni- versal Coverage Scheme (the 30- Baht Scheme) (Coronini- Cronberg et al., 2007). Thus, they did not have to pay for medications prescribed out of pocket. This result contrasts with previous studies by Kronish and Ye (2013) who investi- gated adherence to cardiovascular medications and found that low income was a significant predictor of poor adherence in cardiovascular patients. This was true of other myocardial infarction patients of low financial status also because they had to pay for prescribed medications by themselves (Perreault et al., 2008; Laba et al., 2013).
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Myocardial infarction and nocturnal hypoxaemia

Myocardial infarction and nocturnal hypoxaemia

Objecive The aim of this study was to evalute the influence of nocturnal hypoxaemia on ventricular arrhythmias and myocar- dial ischaemia in patients with myocardial infarction (MI). Method We studied 77 patients (55.8±7.9 years) with MI free of complications, chronic pulmonary diseases, abnormal awake blood gases tension. All patients underwent overnight pulse oximetry and 24-hour electrocardiography. Patients were divid- ed into two groups according to nocturnal hypoxaemia.Total number of ventricular premature complex (VPC); maximal VPC/h; incidence of VPC Lown class>2 and occurrence of ST-segment depression were analysed for nocturnal (10 PM to 6 AM), daytime (6 AM to 22 PM) periods and for the entire 24 hours.
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Risk factors for post-acute myocardial infarction depression in elderly

Risk factors for post-acute myocardial infarction depression in elderly

To that purpose we tried to establish an independent association of some parameters with the occurrence of PSTEMI DD: sex, history of heart disease, arterial hypertension, diabetes mellitus, obesity, lipidic profile, smoking, patient’s socio-economic status and presence of family. Also we studied the correlation of physiopathologic changes, induced by acute myocardial infarction, and DD: ejection fraction of left ventricle (LVEF), Killip classification and heart rhythm disturbances.

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SERUM MAGNESIUM IN ACUTE MYOCARDIAL INFARCTION

SERUM MAGNESIUM IN ACUTE MYOCARDIAL INFARCTION

ABSTRACT: BACKGROUND: In myocardial infarction, there occurs functional deficit of available magnesium due to trapping of free magnesium in adipocytes. Magnesium has been implicated in the pathogenesis of acute myocardial infarction and its complications. Magnesium ions are considered essential for the maintenance of functional integrity of myocardium. The serum magnesium concentration was found to have great significance in acute myocardial infarction. The present study was undertaken to evaluate the prognostic value of serum magnesium in acute myocardial infarction. AIMS AND OBJECTIVES: 1. To evaluate serum magnesium concentration in patients with acute myocardial infarction within 24 hours of presentation and on 7 th day post myocardial infarction. 2. To
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Air pollution effects on myocardial infarction

Air pollution effects on myocardial infarction

RESULTS: Almost 70% of daily hospital admissions due to myocardial infarction were to infirmaries. Despite that, the effects of air pollutants on infarction were higher for intensive care units admissions. All pollutants were positively associated with the study outcomes but SO 2 presented the strongest statistically significant association. An interquartile range increase on SO 2 concentration was associated with increases of 13% (95% CI: 6-19) and 8% (95% CI: 2-13) of intensive care units and infirmary infarction admissions, respectively.

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Arq. Bras. Cardiol.  vol.93 número1

Arq. Bras. Cardiol. vol.93 número1

At the necropsy, the aorta presented moderate to intense atheromatosis, with marked calcification of its abdominal section. The heart presented a globus shape, at the expense of the LV anterior region (Figure 4). Cross-sections of the LV showed intense aneurysmatic dilatation in the LV cavity, the result of a previous extensive transmural myocardial infarction in the septal, anteroseptal, anterior and anterolateral walls, from the basis to the apex, with extensive mural thrombosis, as well as in the inferior wall, from the middle to the apex, with the involvement of approximately 60% of the ventricular muscle (Figure 5). In spite of the presence of cavitary thrombi, no systemic thromboembolism was detected. The histological analysis showed that extensive areas of myocardial tissue had been replaced by fibrosis. The pericardium presented fibrosis, with the parietal and visceral leaflets fastened firmly to each other in the anterior projection of ventricular aneurysm. There were signs of congestive HF represented by hydrothorax to the right and hydroperitoneum, with approximately 360 mL and 480 mL of citrine-yellow fluid, respectively. The dissection and histological analysis of the epicardial coronaries demonstrated severe obstructive atherosclerotic coronary lesions (Figure 6).
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Rev. Col. Bras. Cir.  vol.44 número1

Rev. Col. Bras. Cir. vol.44 número1

23. Task Force on the management of ST-segment ele- vation acute myocardial infarction of the European Society of Cardiology (ESC)., Steg PG, James SK, Atar D, Badano LP, Blömstrom-Lundqvist C, et al. ESC Guidelines for the management of acute myo- cardial infarction in patients presenting with ST-seg- ment elevation. Eur Heart J. 2012;33(20):2569-619. 24. Thiele H, Zeymer U, Neumann FJ, Ferenc M, Olbrich

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