myocardial infarction

A 58-year-old hypertensive man presented to our insti-tution with acute chest pain and dizziness. Electrocardiogram revealed inferior wall myocardial infarction with suspected right ventricular involvement (Figure 1A). Computed tomographic aortography (CTA) depicted ascending aortic dissection (AAD) with involvement of bilateral carotid, subclavian, and right common iliac arteries (Figure 1B). Replacements of aortic valve and ascending aorta with CABG (Ao-RSVG1-LAD and Ao-RSVG2-RCA) were conducted. 

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.

Obesity is a chronic and metabolic disease with a high increasing prevalence worldwide. It has multifactorial pathogenesis including genetic and behavioral factors [1-5]. Overweight and obesity have been defined and classified by the World Health Organization (WHO) and the National Institutes of Health (NIH) [2,3]. A person with a normal weight has Body Mass Index (BMI) of 18.5-24.9. A person with a BMI under 18.5 is called underweight. An adult having a BMI of 25-29.9 is overweight and pre-obese. Class 1 obesity is defined as a BMI between 30.00-34.99. Class 2 (Severe) Obesity is to have a BMI between 35.00-39.99. Morbid (Extreme, Class 3) obesity is to have a BMI over 40 [1-5]. Obesity is significantly associated with enhanced morbidity and mortality rates. It has also various economic, medical and psychological effects and causes health problems including many systemic diseases, economic costs and burdens, social and occupational stigmatization and discrimination and productivity loss [4-6]. Obesity carries the increased risk of development of many systemic and chronic diseases, including sleep apnea, depression, insulin resistance, Type 2 (adult-onset) diabetes, Gout and related arthritis, degenerative arthritis, hypertension, dyslipidemia, heart disease such as myocardial infarction, congestive heart failure, or coronary artery disease, polycystic ovary syndrome and reproductive disorders, Pickwickian syndrome (obesity, red face and hypoventilation), metabolic syndrome, non-alcoholic fatty liver disease, cholecystitis, cerebrovascular accident, colonic and renal cancer, rectal and prostatic cancer in males, and gallbladder, uterus and breast cancer in females [6-12]. In recent years, some publications reported that obesity has been strongly associated with some ocular diseases including age-related cataract and maculopathy, glaucoma, and diabetic retinopathy [13-16]. The recent reports demonstrated that the central corneal thickness and intraocular pressure were increased while as mean thickness of RNFL and retinal ganglion cell and choroidal thickness (CT) were decreased in the morbidly obese subjects [17-19]. However, another study has reported that CT increased in obese children [20]. On the other hand, a recent study reported that all values of the specific tests used to evaluate the ocular surface were within the normal range [21]. In some experimental studies, it has been demonstrated that obesity may cause retinal degeneration [22,23]. Additionally, in a past meeting presentation, it has been speculated that keratoconus is associated with severe obesity [24]. Teorically, idiopathic intracranial hypertension, and papilledema may also be associated with obesity [25]. Obesity may be also a cause of mechanical eyelid abnormalities such as entropion [26]. However, further investigations are needed to detect the significant relationship between these diseases and obesity. On the other hand, the ocular surgeries of obese patients are difficult compared to normal weight-subjects. The posterior capsule rupture and vitreous loss may easily develop during cataract surgery of these patients because obese patients have an elevated vitreous pressure and operating table cannot often be lowered or surgeon’s chair cannot be elevated sufficiently to provide the clear viewing of the operating area and tissues. So, some different surgical manipulations such as standing phacoemulsification technique and reverse Trendelenburg position have been developed. Additionally, the standing vitrectomy technique has been used for vitreoretinal interventions in morbidly obese patients [27,28]. In conclusion, all obese subjects should be subjected to a completed ophthalmological examination and to relevant clinics for the detection of possible comorbidities and diseases

This study presents the frequency of old myocardial infarctions (OMI), and the frequency of unrecognized myocardial infarction (UMI) in elderly people in a forensic material. It was also examined if predisposing factors of UMI could be identified. Of special interest was also to investigate the value of the police’s records as a source for medical information in a forensic setting. The study is based upon medico-legal autopsies of persons above the age of 60 at the time of death during the period 1999-2003. The study included 325 cardiovascular deaths. Of these, 166 died from OMI. UMI accounted for 123 of these (74%). Most UMI were located in the interventricular myocardial septum and left anterior wall (>60%), but no significant differences could be found between UMI and recognized MIs (RMI). No obvious reason could be found as to why the UMI remained unrecognized. Police records were inferior to the hospitals records, regarding medical information to the pathologist, with information about cardiac disease in about 60%, and with information about OMI in 11-17%. Hospital records supplying information about OMI were found in half the cases. It is concluded that unrecognized myocardial infarction is not uncommon among elderly persons, and with a high risk of sudden death. More emphasis should be put in recognizing OMI in ECGs to attempt to reduce the risk of sudden cardiac death.

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).

The morphological evolution kinetics and instabilities of alpha helical peptide 3.613, which involves large amount of stored torsional elastic deformation energy (3-40 eV/molecule), is formulated by the variational method based on the connection between the rates of internal entropy production and the changes in the global Gibbs free energy, assuming that one has isobaric irreversible processes under the isothermal conditions. The present mesoscopic nonequilibrium thermodynamic approach relies on the fact that the global Gibbs free energy of helical conformation involves not only the bulk Gibbs free energy of the amino-acid back bone structure but also the interfacial Gibbs free energy of the enclosing cylindrical shell or the cage associated with the side-wall molecular branches, and their interactions with the immediate surroundings. The proposed variational analysis applied directly on the proposed macro-model has furnished a nonlinear integral equation in terms of the normalized and scaled internal and external variables. This allows us to track down the motion of the total pitch height of the alpha polypeptide along the well-defined trajectories in the displacement-time space, dictated not only by the initial configuration of the helix but also through the gradients of the global Gibbs free energy of the strained helical conformation as the main driving force. In the negative manifold, there is a well-defined region below the dynamic instability regime, in which the helical conformation can evolve towards the nonequilibrium stationary states by expanding, or contracting, depending upon whether the interfacial free energy and/or the applied stress system are below or above the well-defined thresholds level dictated by the initial pitch height. The highest life time may be realized along that trajectory, which follows up the threshold level of the interfacial specific Gibbs free energy, which is gs = -315 erg/cm2. In the upper region of the negative manifold, the helical conformations are driven by the very large applied uniaxial tension or the negative pressure induced by the thermal expansion, in the range of p > 1GPa and/or the strong negative interfacial free energies [3-4 pH] or their combinations, they show strong kinematic instabilities, which can cause not only the accelerated unfolding phenomenon but also cause large extensions that end up with the catastrophic decimations by ruptures and fragmentations. In the positive manifold, the aging behavior of the polypeptide follows up a S-shape path having rather speedy aging behavior compared to the negative manifold, which is separated from by a well-defined boundary, which represents the isochoric path having longest relaxation times, which can be achieved with great stability. Finally, one could attempt to estimate the upper limit of the relaxation time of aging for the modern hominin, from samples of exceptional preservations, relying on the present nonequilibrium theory as well as on the very limited knowledge on the post-mortem DNA and the present pitch heights of the modern hominin, which is found to be about 25,840 yrs, with a life expectation of 451,800 yrs. These figures are very close to those calculated for Neanderthals (SH), which are found to be 31,820 yrs and 499,100 yrs, respectively.

The SARS-Cov-2 virus was firstly identified in Wuhan, China and caused catastrophic destruction all over the world. COVID-19 virus primarily effects lungs of its hosts and impairs it in number of ways. It can also damage multiple organs like Heart, kidney, endocrine glands, skin, brain and several others. Kidneys are also damaged to a great extent. In Heart it can cause acute coronary syndrome, Heart failure, Myocardial infarction. SARS-CoV-2 effect brain especially psychologically. It also causes serious lymphocyte apoptosis. It also neutralizes human spleen and lymph nodes. SARS-CoC-2 can be harmful for those having already liver diseases. Similarly, SARS-CoV-2 has a direct impact on endocrine glands. It is responsible for the various injurious changes in hormones, causes various diseases like acute pancreatitis, decrease in GH, hypoparathyroidism etc. and lead to cause tissues damage in glands. It also some minor effects on nose, and respiratory pathways. It also has some minor effects on eyes and ears whereas it causes several devastations in GIT.

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.

Stroke and acute myocardial infarction are primary global causes of mortality. Statistical studies have shown that acute myocardial infarction is responsible for around 9 million deaths each year. Ischemic stroke and myocardial infarction have a significant role in global adult physical disabilities. While reperfusion is vital for tissue recovery, it may paradoxically, inadvertently increase damage through oxidative stress, inflammation, and cell death. Early reperfusion procedures are currently the sole therapy to reduce infarct size. There are many mysteries about heart biology. It is not known the source of energy for myocardial tissues. The heart-beating force (120 mm Hg) cannot explain how erythrocytes are impelled through almost 95,000 km of capillaries in less than 5 minutes. A better knowledge of how the heart is oxygenated should allow the development of new therapies.