Background: Left atrial volume (LAV) has been established as a sensitive marker of left ventricular (LV) diastolic function and as an independent predictor of mortality in patients with acute myocardial infarction (AMI). LA remodeling and its determinants in the setting of AMI have not been much studied. Methods: We studied 53 patients with anterior AMI and a relatively preserved LV systolic function, who underwent complete reperfusion and received guidelines guided antiremodeling drug management. LA and LV remodeling were assessed using 2D echocardiography at baseline and 6 months. LAV indexed for BSA (LAVi) was used as the index of LA size and further LA remodeling. Results: LAVi increased signifi cantly at 6 months compared to baseline [28.1 (23.0-34.5) vs 24.4 (19.5- 31.6) ml/m2, p=0.002] following LV end diastolic-volume index change [56.8 (47.6-63.9) vs 49.5 (42.0-58.4) ml/m2, p=0.0003]. Other standard LV diastolic function indices did not show any signifi cant change. Univariateanalysis showed a strong positive correlation of LAVi change with BNP levels at discharge, LV mass index and LV volumes indices change, throughout the follow up period. Multivariate regression analysis revealed that BNP plasma levels was the most important independent predictor of LA remodeling (b-coef.=0.630, p=0.001). Conclusions: Despite current antiremodeling strategies in patients with AMI, LA remodeling is frequently asssociated with LV remodeling. Additionally LAVi change in the mid-term reflects better than standard echocardiographic indices LV diastolic filling impairment.

Background: Due to variations in hospital protocols and personnel availability, individuals with myocardial infarction admitted on the weekend may be less likely to receive invasive procedures, or may receive them with a greater latency than those admitted during the week. Whether or not this occurs, and translates into a difference in outcomes is not established. Method: Using the Nationwide Inpatient Sample (2008-2011) database, we identified all patients admitted with a principle diagnosis of acute myocardial infarction. They were stratified by weekend or weekday admission. Baseline clinical characteristics, procedure utilization and latency to procedure were compared, and logistic regression models were constructed to assess the relationship between these variables and in-hospital mortality. Results: Patient demographics and provider-related characteristics (hospital type, geography) were similar between weekend and weekday admission for myocardial infarction. Adjusted for covariates, we found that the odds of mortality for a weekend admission are 5% greater than for a weekday admission (OR: 1.05; 95% CI: 1.01, 1.09, p=0.009). For the utilization of an invasive procedure, we found that the odds of receiving a procedure for a weekend admission were 12% less than the odds for a weekday admission, adjusted for the other covariates (OR: 0.88; 95% CI: 0.86, 0.91, p<0.001). In addition, we found that the time to procedure was an average of 0.18 days (4.32 hours) longer for weekend admissions compared to weekday admissions (95% CI: 0.16, 0.20, p<0.001). However, we did not observe a significant difference in the overall length of stay for weekend and weekday admissions (0.004 days; 95% CI: -0.04, 0.05, p=0.87). Conclusion: In a large and diverse subset of patients admitted with myocardial infarction, weekend admission was associated with fewer procedures, increased latency to those procedures, and a non-significant trend towards greater in adjusted in-hospital mortality.

Coronary artery aneurysm is commonly defined as a localized dilatation exceeding the diameter of adjacent normal coronary segments by 50% [1]. Coronary artery aneurysms may be fusiform, involving the full circumference of the coronary artery, or saccular, involving only a portion of the circumference [2]. Causes of coronary artery aneurysms include atherosclerosis (accounting for 50% of cases), Kawasaki disease, polyarteritis nodosa, infection, trauma, coronary dissection, percutaneous coronary angioplasty, and congenital malformations [3]. The abnormal blood flow within the coronary artery aneurysm may lead to thrombus formation, embolization, rupture, myocardial ischemia or myocardial infarction [4]. Here we present a case of a giant fusiform coronary artery aneurysm who passed away due to coronary rupture after acute myocardial infarction.

For 51 days, Gaza was pummeled down by the Israeli military in a war known as Operation Protective Edge. During the 50 days (7-7-204 to 28-8-2014) of the Israeli campaign, 2104 Palestinians were killed, including 253 women (12%) and 495 children (24%). According to the UN, at least 69% of Palestinians killed were civilians. It is estimated that 10,224 Palestinians, including 3,106 children (30%) and 1,970 women (19%) were injured. Preliminary estimates indicate that up to 1,000 of the children injured will have a permanent disability and up to 1,500 orphaned children will need sustained support from the child protection and welfare sectors, 17,200 homes destroyed or severely damaged, 58 hospitals and clinics damaged [1]. Major stressful events are well documented to increase the incidence of acute cardiac events [2]. Cardiovascular complications more than doubled during the FIFA World Cup games of 2006 [3]. After the September 11 terrorist attacks, significantly more patients presented with acute myocardial infarction to the hospitals in Brooklyn [4] and New Jersey [5]. We were able to examine the effects of the Isreli attacks on acute STEMI presentations in Gaza city.

This is a review of features in ECG to diagnose the culprit artery responsible for the infarction. Localization of the occluded vessel in acute myocardial infarction is important for many reasons: to know which artery is to dilate and stent; to assess the severity of the lesion; to compare with the echocardiographic area with hypokinesia or akinesia and to differentiate the recent from the old occluded vessel. The ST-segment changes in 12-lead ECG form the basis of diagnosis, management, and prognosis.

Fibrinolytic therapy has become synonymous with tissue plasminogen activator (tPA) based on the belief that tPA alone was responsible for natural fibrinolysis. Although this assumption was belied from the outset by disappointing clinical results, it persisted, eventually causing fibrinolysis to be discredited and replaced by an endovascular procedure. Since time to reperfusion is the critical determinant of outcome, which in acute myocardial infarction (AMI) means within two hours, a time-consuming hospital procedure is ill-suited as first line treatment. For this purpose, fibrinolysis is more fitting. The assumption that tPA is responsible for fibrinolysis is contradicted by published findings. Instead, tPA ‘s function is limited to the initiation of fibrinolysis, which is continued by urokinase plasminogen activator (uPA) and that has the dominant effect. tPA and uPA gene deletion and clot lysis studies showed the activators have complementary functions, requiring both for a full effect at fibrin-specific doses. They are also synergistic in combination thereby requiring lower doses for efficacy. A clinical proof of concept study in 101 AMI patients who were treated with a 5 mg bolus of tPA followed by a 90 minute infusion of prouPA, the native form of uPA. A near doubling of the 24 h TIMI-3 infarct artery patency rate was obtained compared to that in the best of the tPA trials (GUSTO). In further contrast to tPA, there were no reocclusions and the mortality was only 1% [1]. A sequential combination of both activators, mimicking natural fibrinolysis, holds promise to significantly improve the efficacy and safety of therapeutic fibrinolysis.

Background: Primary percutaneous coronary intervention (PCI) of the infarct-related artery (IRA) is the most effective treatment modality in ST-segment elevation myocardial infarction (STEMI). Incidence of no flow is 8.8% - 10% in primary PCI of STEMI patients. Our aim was to study actual incidence and outcome of no flow patients. Methods: Five hundred and eighty primary PCI patients were enrolled and evaluated from 2016 January to 2017 December. We used drug eluting stents in all cases. Majority of our patients (> 90%) presented to emergency six hours after onset of symptoms. There were many patients where there was no flow even after mechanical thrombus aspiration and pharmacological vasodilator therapy. We have studied primary outcome (mortality) of no flow in those patients. Results: There were 44 cases of no flow in our series (7.75%). Involvement of Left anterior descending artery (LAD) was in eighteen patients. Right coronary artery (RCA) was culprit in twenty four cases. Only two cases were seen in LCX territory. One month mortality rate in no flow group was 50% and 6.25% in successful recanalization group. One year mortality was 12.5% in successful recanalization group and 66% in no flow group. Conclusion: Refractory no flow during STEMI intervention is associated with increased incidence of major adverse cardiovascular events (MACE). There is no established strategy to solve this phenomenon.

Acute pancreatitis is inflammation of the pancreas that may be accompanied by a systemic inflammatory response which results in impairment of the functioning of various organs, systems. Pancreatitis associated vascular complications very often cause morbidity and mortality. There are various cardiovascular complications like shock, hypovolemia, pericardial effusion, and sometimes ST–T changes in the electrocardiogram (ECG) presenting as acute myocardial infarction (AMI). Acute myocardial infarction complicating acute pancreatitis has rarely been studied and the exact process of myocardial injury still remains unclear. We here report a case of Acute Pancreatitis associated with acute myocardial Infarction.

Pulmonary embolism (PE) is an age-related disorder which is potentially fatal, but frequently misdiagnosed. However, the true prevalence of pulmonary embolism is unknown. Inaccurate estimates of PE prevalence might, in part, be attributable to underrecognition of atypical presentations of this disorder. If true prevalence is unknown, the positive predictive values of both typical and atypical symptoms and signs of PE will be unreliable. The negative predictive value of those parameters will, likewise, be unreliable. The aim of this review is to make clinicians more aware of atypical manifestations of PE, thereby increasing the likelihood of correct diagnosis and, hence, ascertainment of the true prevalence of PE. The range of atypical manifestations was explored by a literature search, using MEDLINE from 1946 to February 2019, and EMBASE, from 1947 to February 2019, and Pubmed, from February 2014 to February 2019, using the search terms atypical, uncommon, unusual, pulmonary embolism, lung embolism, pulmonary thromboembolism. This search revealed atypical presenting features such as non pleuritic retrosternal pain, abdominal pain, atypical breathing patterns, pulmonary oedema, Dressler’s syndrome, atypical radiographic manifestations, atypical electrocardiographic features, manifestations associated with oxygen saturation of 95% or more, coexistence of acute myocardial infarction and pulmonary embolism, coexistence of thoracic aortic dissection and pulmonary embolism, neurological manifestations other than stroke, paradoxical embolism, acute venous thrombosis of atypical location, and pulmonary embolism with normal D-dimer levels.

Dissecting aortic aneurysm with ST segment elevation, and pulmonary embolism with ST segment elevation are two of a number of clinical entities which can simulate ST segment elevation myocardial infarction. Objective: The purpose of this review is to analyse clinical features in anecdotal reports of 138 dissecting aortic aneurysm patients with STEMI-like presentation, and 102 pulmonary embolism patients with STEMI-like presentation in order to generate insights which might help to optimise triage of patients with STEMI-like clinical presentation. Methods: Reports were culled from a literature search covering the period January 2000 to March 2020 using Googlescholar, Pubmed, EMBASE and MEDLINE. Reports were included only if there was a specification of the location of ST segment elevation and an account of the clinical signs and symptoms. Search terms were “ST segment elevation”,”aortic dissection”, “pulmonary embolism”, “myocardial infarction”, and “paradoxical embolism”. Fisher’s exact test was utilised for two-sided comparison of proportions. Proportion was calculated for each group as the number of patients with that parameter relative to the total number of patients assessed for that parameter. Findings: There were 138 patients with aortic dissection, 91 of whom were either fast-tracked to coronary angiography (81 patients) or fast-tracked to thrombolytic treatment (10 patients). There were 47 patients managed with neither of those strategies. There were 102 patients with pulmonary embolism, 71 of whom were fast tracked to coronary angiography, and 31 who did not receive that evaluation. Compared with their dissecting aortic aneurysm counterparts, those dissecting aortic aneurysm patients initially managed by percutaneous coronary intervention or by thrombolysis were significantly (p = 0.0003) more likely to have presented with chest pain, and significantly (p = 0.018) less likely to have presented with breathlessness. The preferential fast-tracking to coronary angiography prevailed in spite of comparable prevalence of back pain in fast tracked and in non-fast tracked subjects. Use of transthoracic echocardiography was also comparable in the two subgroups of dissecting aortic aneurysm patients. Pulmonary embolism patients fast tracked to percutaneous coronary intervention were significantly (p = 0.0008) more likely to have presented with chest pain than their pulmonary embolism counterparts who were not fast-tracked. The prevalence of paradoxical embolism was also significantly (p = 0.0016) higher in fast-tracked patients than in counterparts not fast-tracked. Cardiac arrest was significantly (p = 0.0177) less prevalent in fast-tracked pulmonary embolism patients than in pulmonary embolism patients who were not fast-tracked. Preferential fast-tracking to coronary angiography prevailed in spite of the fact that prevalence of documented deep vein thrombosis was comparable in fast-tracked subjects and in subjects not fast-tracked. The prevalence of use of transthoracic echocardiography was also similar in fast-tracked pulmonary embolism patients vs counterparts not fast tracked. Overall, however, transthoracic echocardiography had been utilised significantly (p = 0.007) less frequently in dissecting aneurysm patients than in pulmonary embolism patients. Conclusion: Given the high prevalence of STEMI-like presentation in aortic dissection there is a need for greater use of point-of-care transthoracic echocardiography to mitigate risk of inappropriate percutaneous coronary intervention(which might delay implementation of aortic repair surgery) and inappropriate thrombolysis(which might precipitate hemorrhagic cardiac tamponade) (75) during triage of patients presenting with ST segment elevation simulating ST segment elevation myocardial infarction (STEMI). Furthermore, during triage of patients with STEMI-like clinical presentation, the combined use of point-of -care echocardiography and evaluation for deep vein thrombosis will facilitate the differentiation between acute myocardial infarction, STEMI-like aortic dissection, and STEMI-like pulmonary embolism. Among STEMI-like patients in whom DAA has been ruled out by point of care TTE, fast tracking to PCI might generate an opportunity to identify and treat paradoxical coronary artery embolism by thrombectomy. Thereby mitigating the mortality risk associated with coronary occlusion. Concurrent awareness of PE as the underlying cause of paradoxical embolism also generates an opportunity to relieve the clot burden in the pulmonary circulation, either by pulmonary embolectomy or by thrombolysis. Above all, frontline clinicians should have a greater awareness of the syndrome of STEMI-like presentation of aortic dissection and STEMI-like pulmonary embolism so as to mitigate the risk of inappropriate thrombolysis and inappropriate percutaneous coronary angiography which seems to prevail even in the presence of red flags such as back pain (for aortic dissection) and deep vein thrombosis(for pulmonary embolism). 

Highly selective and sensitive detection of cardiac troponin I (cTnI) is a powerful complement to clinical diagnosis of acute myocardial infarction (AMI). In this study, a strategy for cTnI detection was developed by constructing a universal biosensing interface composed of zwitterionic peptides and aptamers. The peptides were self-assembled onto gold chips, and some of them were biotinylated. The cTnI-specific binding aptamers were immobilized through the streptavidin-biotin system. Surface plasmon resonance (SPR) measurements revealed the preparation process. The developed aptasensor presents a linear detection with cTnI ranging from 20 ng/ml to 600 ng/ml and a detection limit of 20 ng/ml. The high immobilization of the aptamer enhances the sensitivity of the aptasensor and the calculated KD was 6.75 nM. Due to the outstanding antifouling property of the zwitterionic peptide, the developed aptasensor possesses a high resistance towards protein fouling. Moreover, the aptasensor has excellent selectivity and specificity towards cTnI in complex media. Hence, the proposed peptide-based aptasensor shows great potential for practical application in medium sized Myocardial Infarction (MI).

Background: The concurrent occurrence of acute ischemic stroke and acute myocardial infarction is an extremely rare emergency condition that can be lethal. The causes, prognosis and optimal treatment in these cases are still unclear.Methods: We conducted the literature review and 2 additional cases at Al-Shifa Hospital, we analyzed clinical presentations, risk factors, type of myocardial infarction, site of stroke, modified ranking scale and treatment options. We compare the mortality rate among patients with combination intervention treatment (both percutaneous coronary intervention for coronary arteries and mechanical thrombectomy for cerebral vessels) and medical treatment at the hospital and 90 days after stroke. Results: In addition to our cases, we identified 94 cases of concurrent cardio-cerebral infarction from case reports and series with a mean age of 62.5 ± 12.6 years. Female 36 patients (38.3%), male 58 patients (61.7%). Only 21 (22.3%) were treated with combination intervention treatment.The mortality rate at hospital discharge was (33.3%) and the mortality rate at 90 days was (49.2%). In patients with the combination intervention treatment group: the hospital mortality rate was 13.3% and the 90-day mortality rate was: 23.5% compared with the mortality rate in medical treatment (23.5% at the hospital and 59.5% at 90 days (p value 0.038 and 0.012 respectively) Conclusion: Concurrent cardio-cerebral infarction prognosis is very poor, about a third of patients died before discharge and half of the patients died 90 days after stroke. Despite only one-quarter of patients being treated by combination intervention treatment, this treatment modality significantly reduces the mortality rate compared to medical treatment.

Between coronary artery anomalies, myocardial bridging means an epicardial coronary artery, mostly left anterior descending artery (LAD), running through an intramyocardial “tunnel” (usually in the middle segment), leading during systolic contraction, flow reduction, through the vessel. When this anomaly is associated with a coronary fistula, which “steals” more from the bloodstream, the symptoms are more pronounced, and the management complex is surgical in particular. Despite the presence from birth remains asymptomatic and it becomes clinically manifest later in the third to fourth decade of life, with a diverse palette of symptoms; angina, arrhythmias, and acute myocardial infarction up to sudden death. Diagnosis and particular management, medical, interventional, and surgical should avoid major cardiac complications and sudden death. We present two adult patients, with coronary artery bridging, one case associated with coronary artery fistula, LAD to pulmonary artery trunk, very symptomatic with surgical management, and the second only myocardial bridging controlled with medication and supervision.

Background: Acute Myocardial Infarction (AMI) results in a reduction in patients’ life expectancy. Different risk factors affect the risk of Major Adverse Cardiac Events (MACE). Although the role of kidney dysfunction in patients with Chronic Kidney Disease (CKD) in cardiac events has been identified, many patients with AMI are unaware of their underlying kidney disease. This study aimed to compare the incidence of adverse cardiovascular events and identify predictors of major adverse cardiovascular events in the medium term among patients with and without renal dysfunction following AMI. Methods: This retrospective cohort study was conducted on 1039 patients who were hospitalized for Acute Myocardial Infarction (AMI) between 2018 and 2019. The patient cohort comprised 314 women (mean age: 69.8 ± 13.2 years) and 725 men (mean age: 60.5 ± 13.8 years). Patient data were obtained from the registry of patients with acute myocardial infarction and the participants were followed up for a minimum of one year following hospital discharge to assess the incidence of MACE.Results: The study found that patients with a Glomerular Filtration Rate (GFR) level below 60 had a significantly higher mortality rate than those with a GFR level of 60 or above (15.7% vs. 3.5%,p < 0.0001). The multivariate analysis showed that Diabetes Mellitus (DM), GFR, and Non-ST Elevation Myocardial Infarction (NSTEMI) are significant risk factors for cardiovascular events. (p = 0.016, p = 0.015, p = 0.006 respectively), while variables such as sex, age, and Hypertension (HTN) were not significant risk factors. There was a negative correlation between GFR and death (0.241 - = r, p < 0.0001)Conclusion: This study highlights the importance of detecting kidney disease during an AMI and managing risk factors for cardiovascular disease to improve health outcomes and reduce the risk of mortality.