Ischemic Abnormalities Research Articles

Modeling creatine-kinase MB concentrations following coronary artery bypass grafting

BackgroundAn increase in cardiac biomarkers is a prerequisite for diagnosing periprocedural myocardial infarction (PMI) after coronary artery bypass grafting (CABG). Early-phase risk detection may be aided by modeling time-dependent serum creatine kinase-MB (CK-MB) concentrations. This study aimed to model the kinetics of CK-MB while identifying its influencing factors. MethodsPatients who underwent elective CABG and had CK-MB measurements within 72 hours postoperatively were included. The primary outcome was the modeled post hoc kinetics of CK-MB in patients without potential PMI. These patients were defined as having no potential PMI based on the absence of ischemic electrocardiographic abnormalities, imaging abnormalities, in-hospital cardiac arrest, mortality, or postoperative unplanned catheterization. A web-based application was created using mixed-effect modeling to provide an interactive and individualized result. ResultsA total of 1589 CK-MB measurements from 635 patients who underwent elective isolated CABG were available for analysis. Of these, 609 patients (96%) had no potential PMI and 26 (4%) had potential PMI. Male sex, aortic cross-clamp time, and cardioplegia type significantly impacted CK-MB concentrations. The diagnostic accuracy of the model had an area under the receiver operating characteristic curve of 82.8% (95% confidence interval, 72.6%-90.2%). A threshold of 7 μg/L yielded a sensitivity of 94% and a specificity of 80% (positive predictive value, 17%; negative predictive value, 99%) for excluding potential PMI in our study population. ConclusionsCK-MB release after CABG depends on the timing of measurement, patient sex, aortic cross-clamp time, and cardioplegia type. The model (available at https://www.cardiomarker.com/ckmb) can be validated, reproduced, refined, and applied to other biomarkers.

Abstract 12289: A Postpartum Diastolic Murmur

A 44-year-old G3P1011 underwent uncomplicated Caesarian section for obstetric indications with delivery of a healthy girl. Several hours postpartum, she developed hypoxemia requiring transient supplemental oxygen. Cardiology was consulted for further evaluation. Upon initial assessment, she appeared comfortable with an oxygen saturation of 93% on room air. She reports an otherwise uneventful pregnancy. Her past medical history is significant for chronic hypertension on propranolol. She was afebrile with a HR of 91, BP 147/66 (left arm) and 155/68 (right arm). Her JVP was 10-11 cm H20. There was a III/IV low-pitched decrescendo early-mid diastolic murmur, loudest at the left lower sternal border, radiating to the apex, and a systolic ejection murmur. EKG (panel A) showed normal sinus rhythm, with no ischemic abnormalities. Due to the discovery of a new murmur, there was concern for valvular pathology as a cause for her suspected heart failure, particularly aortic regurgitation (AR). An urgent TTE (panel C-E) was requested and showed a dissection flap in the ascending aorta, effacement of the sinotubular junction, and severe AR. CT angiogram confirmed the diagnosis of type A aortic dissection (AD; panel B). Twelve hours after the delivery of her baby, she underwent emergent aortic valve repair and aortic arch replacement. She recovered well and was discharged home post-op day 6. Though no human data exists, animal data suggests increased AD risk in breastfeeding animals with Marfan Syndrome. Due to her near catastrophic presentation, she elected to not breastfeed. Her genetic testing results are pending. AD in pregnancy is rare. There is an increased risk of AD in pregnant compared to non-pregnant women. AD often occurs in the third trimester or postpartum, and most women are unaware of a preexisting arteriopathy. In this case, the detection of a diastolic murmur resulted in rapid diagnosis and treatment, essential in the management of this life-threatening condition.

Is later-life depression a risk factor for Alzheimer’s disease or a prodromal symptom: a study using post-mortem human brain tissue?

BackgroundDepression and dementia are both common diseases. Although new cases of depression are more common in younger adults, there is a second peak at the age of 50 years suggesting a different pathological process. Late-life depression (LLD) is associated with dementia. However, it remains unclear whether depression represents a dementia prodrome or is a true risk factor for its development.LLD is thought to have a vascular component and this may be a possible link between depression and dementia. We hypothesised that later-life depression is a prodromal manifestation of dementia and would therefore be associated with more AD, and/or ischaemic brain abnormalities that are present in earlier-life depression or in age- and sex-matched controls.MethodsWe assessed post-mortem orbitofrontal cortex and dorsolateral pre-frontal cortex from 145 individuals in 4 groups: 28 18–50-year-olds with depression, 30 older individuals (ages 51–90) with depression, 28 with early AD (Braak tangle stages III–IV) and 57 matched controls (17 early-life, 42 later-life). Levels of Aβ, phospho-tau and α-synuclein were assessed by immunohistochemistry and ELISA. To quantify chronic ischaemia, VEGF, MAG and PLP1 were measured by ELISA. To assess pericyte damage, PDGFRB was measured by ELISA. For blood–brain barrier leakiness, JAM-A, claudin 5 and fibrinogen were measured by ELISA. To quantity endothelial activation, the ratio of ICAM1:collagen IV was assessed by immunohistochemistry.ResultsThere was no evidence of chronic cerebral hypoperfusion or increased Aβ/tau in either depression group. There was also no indication of pericyte damage, increased blood–brain barrier leakiness or endothelial activation in the OFC or DLPFC in the depression groups.ConclusionsContrary to some previous findings, we have not found evidence of impaired vascular function or increased Aβ in LLD. Our study had a relatively small sample size and limitations in the availability of clinical data. These results suggest that depression is a risk factor for dementia rather than an early manifestation of AD or a consequence of cerebral vascular insufficiency.

Crosstalk between genetic variability of adiponectin and leptin, glucose-insulin system and subclinical atherosclerosis in patients with newly diagnosed type 2 diabetes. The Verona Newly Diagnosed Type 2 Diabetes Study 14.

To evaluate the relationship of genetic variability of adiponectin (ADIPOQ), leptin (LEP) and leptin receptor (LEPR) genes with glucose-insulin system and markers of subclinical atherosclerosis (ATS) in patients with newly diagnosed type 2 diabetes. In 794 subjects we performed: 1) euglycemic hyperinsulinemic clamp to assess insulin sensitivity; 2) mathematical modelling of a 5h-OGTT to estimate β-cell function; 3) resting ECG; 4) carotid artery and lower limb artery eco-doppler sonography to identify ATS; 5) genotyping of tag-SNPs within ADIPOQ, LEP and LEPR gene. Regression analyses showed: 1) adiponectin levels were negatively associated with BMI, waist-to-hip ratio and triglycerides and positively with HDL and insulin sensitivity (p-all<0.03); 2) leptin levels were positively associated with BMI, HDL-cholesterol and plasma triglycerides and negatively with insulin sensitivity (p-all<0.001). Two SNPs (rs1501299 and rs2241767) within ADIPOQ gene were associated with circulating levels of adiponectin. The ADIPOQ-GAACA haplotype was associated with plasma adiponectin (p=0.034; β=-0.24), ECG abnormalities (p=0.012; OR=2.76), carotid ATS (p=0.025; OR=2.00) and peripheral limb artery ATS (p=0.032; OR=1.90). The LEP-CTA haplotype showed an association with ischemic ECG abnormalities (p=0.017; OR=2.24). Finally, LEPR-GAACGG was associated with circulating leptin (p=0.005; β=-0.31) and worst β-cell function (p=0.023; β=-15.10). Omnibus haplotype analysis showed that ADIPOQ haplotypes were associated with levels of adiponectin and common carotid artery ATS, LEP with peripheral limb artery ATS, whereas LEPR haplotypes influenced circulating levels of leptin. Results of this study reinforce knowledge on adipokines' role in regulating glucose metabolism; in particular highlighted the potential atherogenic role of leptin and the anti atherogenic role of adiponectin.

P35 CARDIAC MAGNETIC RESONANCE: PROMISING SOLUTION IN CLINICAL DILEMMA

Abstract There are many clinical conditions in which symptoms and signs can overlap, resulting in a real "clinical dilemma". Differential diagnosis is essential for identifying the pathology affecting a patient and consequently making the best therapeutic decisions. Herein we report a case of a young patient, with strong smoking habit, who looked for medical attention after experiencing chest pain, associated to upper airways inflammation. EKG revealed ischemic abnormalities, echocardiography showed a preserved ejection fraction (EF: 55%) and global cardiac contractility, although akinesia of the mid–segment of the inferolateral wall, and the presence of a mild inferolateral pericardial effusion. A concomitant increase in myocardial necrosis enzymes and inflammatory markers was observed in blood tests, but the coronarography showed undamaged coronary arteries. This clinical picture characterized by the young age of the patient, by the intercurrent inflammatory event, by the presence of pericardial rubbing on physical examination, by the evidence of echocardiographic end EKG anomalies in the absence of documentable epicardial lesions and by the complete symptomatic remission after anti – inflammatory therapy with acetylsalicylic acid and Colchicine was highly suggestive of pseudoinfarct–presenting myopericarditis. To confirm such diagnosis, cardiac magnetic resonance (CMR) was requested, unexpectedly, it showed oedema on the mid–basal inferolateral T2–weighted STIR sequences, but also microvascular obstruction (MVO) on early EGE contrastographic sequences mid–basal inferolateral site, and finally evidence of transmural fibrosis in the same site to the DE sequences resulting in pathognomonic lesions for acute ischemia in absence of epicardial coronaropathy. CMR imaging, which is able to analyse cardiac structure and function and simultaneously provide tissue characterization, has been an essential investigation for the diagnosis of MINOCA, as CMR can readily pinpoint many conditions responsible for myocardial damage and allow pathological discrimination of patients. Our patient‘s final diagnosis was “STEMI, MINOCA, and concomitant pericarditis” implying a consequent therapeutic modification, introducing DAPT. Making differential diagnosis in similar clinical conditions characterized by overlapping presentations, allows the use of personalized therapeutic strategies for each patient and better final results.

Sirtuin-3 activates the mitochondrial unfolded protein response and reduces cerebral ischemia/reperfusion injury.

Sirtuin-3 (Sirt3) deacetylates several mitochondrial proteins implicated into cerebral ischemia/reperfusion (I/R) injury. The mitochondrial unfolded protein response (UPRmt) favors mitochondrial proteostasis during various stressors. Here, we used Sirt3 transgenic mice and a transient middle cerebral artery occlusion model to evaluate the molecular basis of Sirt3 on the UPRmt during brain post-ischemic dysfunction. The present study illustrated that Sirt3 abundance was suppressed in the brain after brain ischemic abnormalities. Overexpression of Sirt3 in vivo suppressed the infarction size and attenuated neuroinflammation after brain I/R injury. Sirt3 overexpression restored neural viability by reducing mitochondrial ROS synthesis, maintaining the mitochondrial potential and improving mitochondrial adenosine triphosphate synthesis. Sirt3 overexpression protected neuronal mitochondria against brain post-ischemic malfunction via eliciting the UPRmt by the forkhead box O3 (Foxo3)/sphingosine kinase 1 (Sphk1) pathway. Inhibiting either the UPRmt or the Foxo3/Sphk1 pathway relieved the favorable influence of Sirt3 on neural function and mitochondrial behavior. In contrast, Sphk1 overexpression was sufficient to reduce the infarction size, attenuate neuroinflammation, sustain neuronal viability and prevent mitochondrial abnormalities during brain post-ischemia dysfunction. Thus, the UPRmt protects neural viability and mitochondrial homeostasis, and the Sirt3/Foxo3/Sphk1 pathway is a promosing therapeutic candidate for ischemic stroke.

286 A CASE REPORT OF TYPE II KOUNIS SYNDROME

Abstract Case presentation and management A 81-years old female presented to the emergency department of our hospital with dyspnea and chest pain. She had a history of chronic kidney disease and left bundle brunch block (LBBB) never further investigated. Non diagnostic ECG was performed in the setting of pre-existing LBBB. HS-T-Troponin level was significantly elevated (986 ng/L). A transthoracic echocardiogram (TTE) revealed inferior and posterior wall hypokinesis. NSTEMI was diagnosed and coronary angiography via the femoral artery revealed subocclusive stenosis of the right coronary artery (RCA) and 80% stenosis of left anterior descending artery (LAD). Coronary stent positioning was performed for the RCA culprit lesion and staged complete revascularization was planned. Complications After two days, the patient experienced sharp pain in the right groin and a femoral pseudoaneurysm was diagnosed by Ultrasound Color Doppler. Subsequently anemia suggested the development of retroperitoneal hematoma but it was excluded by contrast CT. Unfortunately, the patient developed acute chest pain, wheezing and erythematous pruritic rash 10 minutes after injection of contrast medium agent. The ECG didn't show any new ischemic abnormalities in the setting of pre-existing LBBB. The peak CK- MB level was significantly elevated (87 ng/mL). New onset apical region akinesia and anterior wall hypokinesia were detected on TTE. Acute coronary syndrome (ACS) was suspected consistent with symptoms, new onset wall motion abnormalities and CK-MB elevations. The patient was diagnosed with allergic reaction and coronary vessel spasm secondary to contrast agent injection in pre-existing atherosclerotic plaque. Due to the high probability of an hypersensitivity reaction to the contrast medium agent we did not perform a new coronary angiography to confirm the diagnosis. Promethazine, Urbason and Nitroglicerin were administered with clinical improvement. The next day we observed recovery of the anterior and apex wall motion abnormalities consistent with coronary vessel spasm. Echocardiographic wall motion abnormalities before and after coronary spasm: Take home message We presented the case of an allergic reaction leading to the release of inflammatory mediators responsible of coronary vessel spasm causing acute myocardial infarction. It can also be induced by injection of contrast medium like in the presented case. Therefore, clinicians and radiologist should recognize this rare but critical disease to ensure prevention and appropriate management.

253 EXCERCISE-INDUCED PULMONARY HYPERTENSION AND CORONARY ARTERY ANOMALY: AN UNUSUAL ASSOCIATION

Abstract A healthy 55-year-old competitive sportsman, with familial history of early sudden cardiac death, came to our attention following the finding of asymptomatic exercise-induced myocardial ischemia (ST depression in V3- V6). Computed tomography (CT) coronary angiogram excluded atherosclerotic disease but showed a dominant right coronary artery (RCA) originating from left Valsalva sinus and with an interarterial course between the ascending aorta and the pulmonary artery. Both the trunk of the pulmonary artery and the right ventricle were reported as mildly dilated Transthoracic echocardiography showed a normal left ventricle (LV), while confirmed right ventricle (RV) dilatation, moderate tricuspid regurgitation (TR) and interatrial septal aneurysm. Stress echocardiography excluded inducible ischemia, but highlighted exercise-induced pulmonary hypertension (PH) (PAPs 25 → 70 mmHg), while a transesophageal echo confirmed a left-to-right shunt due to a 8-mm Patent Foramen Ovale (PFO). Rheumatological, thromboembolic and parenchymal lung diseases were excluded as possible causes of exercise-induced PH; a rest right heart catheterization (RHC) showed a Qp/Qs ratio at the upper limits of normal range without PH. Nuclear stress testing identified trivial asymptomatic septal ischemia. The patients started medium dose of beta-blockers and early follow-up was planned. This clinical case raises some questions: why is RV dilated? What role does PFO play? What is the cause of the inducible ischemia? What is the pathogenesis of exercise-induced PH? Pulmonary Arterial Hypertension, in early stages, often manifests only under exertion, but it is usually characterized by exercise dyspnea and low oxygen saturation. Moreover, intracardiac shunts may be involved in developing PH. In this specific case, pulmonary trunk may be expanded by pressure overload, causing the compression of aberrant RCA and consequent ischemic abnormalities. RV dilatation might be explained by exercise-induced PH itself, but it was not severe and has to be demonstrated by exercise right heart catheterization. The main questions are: which is the primary etiology of right chamber enlargement and myocardial ischemia? Which is the most appropriate therapeutic approach (i.e. conservative vs interventional)?

Electrocardiographic findings and prognostic values in patients hospitalised with COVID-19 in the World Heart Federation Global Study

BackgroundCOVID-19 affects the cardiovascular system and ECG abnormalities may be associated with worse prognosis. We evaluated the prognostic value of ECG abnormalities in individuals with COVID-19.MethodsMulticentre cohort study with adults...

ECG abnormalities and their relation to COVID-19 outcomes – a WHF study

Abstract Introduction COVID-19 is a respiratory tract infection caused by the Coronavirus (SARS-CoV-2) and its main clinical manifestations are respiratory. The cardiovascular system can also be affected, especially in patients with severe acute respiratory syndrome [1]. On the other hand, cardiovascular disease (CVD) and risk factors have been shown to be predictors of poor outcomes in COVID-19 [2]. Diverse electrocardiographic abnormalities can be found in this condition [3], although their value as a prognostic predictor have not been properly established due to heterogeneity in abnormalities evaluation and small sample sizes in related studies [4]. Purpose The aim of the present study is to evaluate the association of electrocardiogram (ECG) findings to poor COVID-19 outcomes Methods This is a multicentric cohort study that followed hospitalized adults due to COVID-19, from low-middle and high-income countries as part of the World Heart Federation (WHF) Global Study on CVD and COVID-19 initiative [5]. Participants were followed up from hospital admission until 30 days post discharge. For the present study, participants with a valid ECG were included. ECG findings were described according to standardized measurements [heart rate, PR interval, QRS duration and axis, corrected QT interval (QTc)] and abnormalities (according to the Minnesota code system). Abnormalities utilized were grouped into ischemic abnormalities (q waves and ST-T abnormalities), atrial fibrillation (AF), prolonged QTc, sinus tachycardia (defined for the study as above 120 bpm), right and left bundle branch block and presence of any major abnormality. The primary outcome was defined as death from any cause. The secondary outcomes were intensive care unit (ICU) admission and cardiovascular events (myocarditis, pericarditis, myocardial infarction, acute heart failure, ischemic and hemorrhagic stroke). Multiple logistic regression was used to evaluate the association of ECG abnormalities to the outcomes of interest. Adjustments were made in a step by step fashion including gender, age, country of residence, cardiovascular risk factors (diabetes, hypertension, tobacco use) and presence of comorbidities (CVD, asthma, cancer, immunosuppression and chronic kidney disease). Results The clinical characteristics of the cohort are described in table 1. Figure 1 represents the odds ratio and its 95% confidence interval of having the defined outcomes when presenting a ECG abnormality for the final regression model. Conclusion ECG abnormalities were independently related to poor outcomes in COVID-19 after accounting for multiple confounders. Significant associations were more frequently found for ischemic abnormalities, heart rate above 120 bpm, atrial fibrillation and having at least one major electrocardiographic abnormality. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): Pfizer and Sanofi PasteurWorld Heart Federation

Feasibility of prehospital identification of non-ST-elevation myocardial infarction by ECG, troponin and echocardiography

BackgroundPrehospital identification and selection of treatment strategy in patients with suspected non-ST-elevation myocardial infarction (NSTEMI) is challenging. The aim of this study was to evaluate the feasibility and diagnostic accuracy...

Myocardial infarction in the population of some Russian regions and its prognostic value

Aim. To study the prevalence of myocardial infarction (MI) in the population of Russian regions and its contribution to cardiovascular events.Material and methods. The analysis material was representative samples of the population aged 35-64 years from 11 Russian regions, examined within the multicenter study “Epidemiology of Cardiovascular Diseases and their Risk Factors in Regions of Russian Federation”. The response rate was about 80%. The study used a community-based systematic stratified multiply random sample. During the study, information on prior MI was obtained using a standard questionnaire. Anthropometry and measurement of blood pressure (BP) and heart rate (HR) with an automatic BP monitor were performed. Resting electrocardiography (ECG) was performed, followed by Minnesota coding. Major and minor QQS waves and STT segments were considered as ischemic ECG abnormalities. Biochemical parameters were determined using an Arkhitect 000 Clinical Chemistry Analyzer. The median prospective follow-up was 6,21 [5,25; 6,75] years. A composite endpoint (CE) was analyzed, including cardiovascular death and non-fatal MI. During the follow-up period, 363 all-cause deaths were detected, of which 134 were from cardiovascular diseases, while 196 — CEs. Statistical analysis was carried out in R 3.6.1 environment.Results. The MI prevalence among the Russian population was 2,9%; 5,2% for men and 1,5% for women, increasing with age. Men with prior MI were more likely to take statins and beta-blockers than women as follows: 39,0% vs 25,6% and 29,3% vs 27,1%, respectively. MI newly diagnosed within the follow-up period was associated with the following risk factors (RFs): smoking, increased BP, HR, triglycerides and glucose. For individuals with prior MI, a significant relationship was found only with smoking. Multiple comparison of the contribution of RFs, ECG abnormalities, and prior MI showed that the inclusion of ischemic ECG abnormalities in the analysis significantly increases the risk of cardiovascular events in individuals without prior MI compared with individuals without both MI and ECG changes. A high CE risk was noted in patients with prior MI: relative risk (RR), 4,73 (2,92-7,65); the addition of ischemic ECG abnormalities increased the RR to 5,75 (3,76-8,8).Conclusion. The RR of CEs in patients with prior MI without or with ischemic ECG changes is 4,73 and 5,75 times higher than in patients without MI and ECG abnormalities. The risk factors identified in this case cannot explain such an increase in CEs. It is obvious that people with prior MI need rehabilitation. The presence of RFs in patients with newly diagnosed MI indicates insufficient primary prevention, which suggests that strengthening preventive measures to eliminate conventional risk factors in patients with newly diagnosed MI will help reduce the risk of recurrent MI or cardiovascular mortality.

Coronary microvascular dysfunction: mechanisms and clinical outcome

A large percentage of patients, predominantly female, who undergo coronary angiography for typical chest pain do not have significant coronary stenosis. Many of these patients with microvascular myocardial disease have left ventricular hypertrophy, cardiomyopathies, valve disease, or other clinical conditions. The definition of microvascular angina is based on (i) symptoms of myocardial ischemia, (ii) absence of obstructive coronary artery disease (<50% stenosis on coronary angiography or coronary computed tomography scan), (iii) objective evidence of myocardial ischemia (ischemic electrocardiographic abnormalities during episodes of chest pain and/or myocardial perfusion defects or regional contractility abnormalities), and (iv) pathological indices of microcirculation (index of microcirculatory resistance >25, coronary flow reserve <2.0) and/or microvascular spasm (TIMI flow <2) during intracoronary vasoreactivity tests. The basic mechanisms and the diagnostic tests of microvascular dysfunction are reported in detail.From a clinical standpoint, while the crucial role of microcirculation in determining short- and long-term prognosis is evident, efforts to date to improve clinical outcomes in patients with microvascular obstruction have had limited success, most likely because microvascular dysfunction is a multifactorial process with several interdependent underlying pathophysiological mechanisms. Therefore, further studies are needed to develop effective therapeutic strategies for microvascular myocardial disease.

P195 A CASE REPORT OF TYPE TWO KOUNIS SYNDROME

Abstract A 81–years old female presented to the emergency department of our hospital with dyspnea and chest pain. She had a history of chronic kidney disease and left bundle brunch block (LBBB) never further investigated. Non diagnostic ECG was performed in the setting of pre–existing LBBB. HS–T–Troponin level was significantly elevated (986 ng/L). A transthoracic echocardiogram (TTE) revealed inferior and posterior wall hypokinesis. NSTEMI was diagnosed and coronary angiography via the femoral artery revealed subocclusive stenosis of the right coronary artery (RCA) and 80% stenosis of left anterior descending artery (LAD). Coronary stent positioning was performed for the RCA culprit lesion and staged complete revascularization was planned. After two days, the patient experienced sharp pain in the right groin and a femoral pseudoaneurysm was diagnosed by Ultrasound Color Doppler. Subsequently anemia suggested the development of retroperitoneal hematoma but it was excluded by contrast CT. Unfortunately, the patient developed acute chest pain, wheezing and erythematous pruritic rash 10 minutes after injection of contrast medium agent. The ECG didn’t show any new ischemic abnormalities in the setting of pre–existing LBBB. The peak CK–MB level was significantly elevated (87 ng/mL). New onset apical region akinesia and anterior wall hypokinesia were detected on TTE. Acute coronary syndrome (ACS) was suspected consistent with symptoms, new onset wall motion abnormalities and CK–MB elevations. The patient was diagnosed with allergic reaction and coronary vessel spasm secondary to contrast agent injection in pre–existing atherosclerotic plaque. Due to the high probability of an hypersensitivity reaction to the contrast medium agent we did not perform a new coronary angiography to confirm the diagnosis. Promethazine, Urbason and Nitroglicerin were administered with clinical improvement. The next day we observed recovery of the anterior and apex wall motion abnormalities consistent with coronary vessel spasm. Take Home Message We presented the case of an allergic reaction leading to the release of inflammatory mediators responsible of coronary vessel spasm causing acute myocardial infarction. It can also be induced by injection of contrast medium like in the presented case. Therefore, clinicians and radiologist should recognize this rare but critical disease to ensure prevention and appropriate management.

MRI findings in COVID-19 positive and COVID-19 negative patients presenting with acute neurological symptoms – a case-control study

Background &amp; Objective: Neurological manifestations of novel-coronavirus disease (COVID-19) have been described in various studies. None of these studies has compared the findings in COVID-19 patients with COVID-negative patients presenting with similar clinical symptomatology during the same period. We undertook this case-control study with an aim to establish a direct relationship between COVID-19 infection and CNS related clinical and imaging presentations. Methods: This study was a review of retrospectively collected data of the patients who presented with different neurological symptoms to a tertiary care hospital in India. Based on results of Reverse transcriptase-polymerase chain reaction for SARS-Co-V-2, patients were classified into COVID-19 positive and COVID-19 negative groups. MRI findings in both groups were reviewed for acute ischemic stroke, intracranial bleed and other acute imaging abnormalities. Basic demographic information and stroke-related co-morbidities were also compared. Results: Eighty four patients in COVID-19 positive group and 323 patients in COVID-19 negative group underwent brain MRI for acute neurological symptoms during the same period. There was no statistically significant difference in presenting symptoms, sex distribution and risk factors for stroke. There was a higher prevalence of increased coagulability in COVID-19 positive group (p-value = 0.009). No statistically significant association was observed for infarcts or their hemorrhagic transformation, intracranial bleed, intracranial infection or dural sinus thrombosis. An association was found between acute diffuse leukoencephalopathy and COVID-19 infection (p value &lt; 0.05). Conclusion: The current study points towards a weak direct association between COVID-19 infection and acute abnormalities in MRI brain studies, especially in patients with pre-existing co-morbidities.

Long-term outcomes in patients with acute myocardial infarction and no ischemic changes on electrocardiogram

BackgroundAcute myocardial infarction (MI) is commonly associated with ischemic abnormalities on electrocardiography (ECG). However, a significant proportion of patients present with no ischemic changes (NIC), and their baseline characteristics and management differ considerably from those with other ECG patterns. In the era of rapid troponin assays, the exact prognostic effects of normal ECGs remain unclear. ObjectivesThis study aimed to compare the outcomes of patients with MI without ischemic changes and those with other ECG patterns. MethodsBetween 2012 and 2018, 155,073 patients with MI were enrolled in the prospective nationwide Polish Registry of Acute Coronary Syndromes (PL-ACS). The patients were assigned to one of the following groups: NIC, ST-segment elevation (STE), ST-segment depression (STD), T-wave inversion (TWI), and other ST-T abnormalities (STT). ResultsThe NIC group accounted for 9.56% of all patients. The in-hospital risk of death was lower in the TWI group than in the NIC group. In the STE, STD, and STT groups, the short-term results were substantially worse. During the 12-month observation period, TWI had the best prognosis. The worst long-term prognoses were associated with STT and STD. The outcomes of the STE and NIC groups were similar (12-month death rate 9.0% vs. 8.7%, respectively; P=0.534), despite the fact STE was an independent predictor of 12-month prognosis. ConclusionsThe prognosis of patients with MI and NIC is not as favorable as previously thought. Their long-term outcomes were equal to those of the TWI and STE MI groups.

Electrocardiographic Abnormalities in Patients With Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Objective: The objective of this article was to determine the frequency of different electrocardiographic (ECG) abnormalities in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD).Design: This is a cross-sectional study.Place and duration: The study was conducted at the medicine department at Civil Hospital Karachi, Pakistan, between November 2018 and May 2019.Method: Both female and male participants aged 18-60 years with acute exacerbation of COPD (as per the operational definition) for more than three days who did not receive any treatment for exacerbation were included in the study. Twelve-lead ECG was recorded (Schiller AG, Baar, Switzerland) for 10 minutes after the supine rest, with a 50 mm/s of paper speed, 10 mm/mV of gain, and filter default settings.Results: In total, 140 participants (male: n = 124 [88.6%] and female: n = 16 [11.4%]) were included the research. The mean age of the participants was 40.43 ± 11.51 years. In terms of severity, 46 (32.95) patients presented with mild, 46 (32.9%) with moderate, and 48 (34.4%) with severe exacerbation. Moreover, 33 (23.65%) participants had ECG abnormalities, i.e., 13 (9.3%) patients presented with right atrial enlargement, and eight (5.7%) with right ventricular hypertrophy. Patients with a longer smoking duration (years) were likely to present with ECG abnormalities.Conclusion: Patients with COPD who had severe acute exacerbation and a long smoking duration have a high prevalence of ECG abnormalities. Hence, ECG may be a valuable tool for detecting ischemic abnormalities among patients with COPD, independent of previously known heart disease, in clinical settings.

No evidence of decreased perfusion or blood‐brain barrier leakiness in later life depression

Depression and dementia are both common diseases. Although new cases of depression are more common in younger adults there is a second peak at the age of 50 years suggesting a different pathological process. Late-life depression (LLD) is associated with dementia. However, it remains unclear whether depression represents a dementia prodrome or is a true risk factor for its development. LLD is thought to have a vascular component and this may be a possible link between depression and dementia. We hypothesised that later-life depression is a prodromal manifestation of dementia and would therefore be associated with more AD, and/or ischaemic brain abnormalities than are present in earlier-life depression or in age- and sex-matched controls.We assessed post-mortem orbitofrontal cortex and dorsolateral pre-frontal cortex from 145 individuals in 4 groups: 28 18-50-year-olds with depression, 30 older individuals (ages 51-90) with depression, 28 with early AD (Braak tangle stages III-IV) and 57 matched controls (17 early-life, 42 later-life). Levels of Aβ, phospho-tau and α-synuclein were assessed by immunohistochemistry and ELISA. To quantify chronic ischaemia, VEGF, MAG and PLP1 were measured by ELISA. To assess pericyte damage, PDGFRB was measured by ELISA. For blood-brain barrier leakiness, JAM-A, claudin 5 and fibrinogen were measured by ELISA and the ratio of ICAM1:collagen IV assessed by immunohistochemistry.There was no evidence of chronic cerebral hypoperfusion or increased Aβ in either depression group. There was also no indication of pericyte damage or increased blood-brain barrier leakiness in the OFC in the depression groups CONCLUSION: Contrary to some previous findings, we have not found evidence of impaired vascular function or increased Aβ in LLD. These results suggest that it is a risk factor for dementia rather than an early manifestation of AD or a consequence of cerebral vascular insufficiency.

The interobserver agreement of ECG abnormalities using Minnesota codes in people with type 2 diabetes.

To assess the interobserver agreement in categories of electrocardiogram (ECG) abnormalities using the Minnesota Code criteria. We used a random sample of 180 ECGs from people with type 2 diabetes. ECG abnormalities were classified and coded using the Minnesota ECG Classification. Each ECG was independently rated on several abnormalities by an experienced rater (rater 1) and by two cardiologists (raters 2 and 3) trained to apply the Minnesota codes on four Minnesota codes; 1-codes as an indication for myocardial infarction, 4 en 5-codes as an indication for ischemic abnormalities, 3-codes as an indication for left ventricle hypertrophy, 7-1-codes as an indication for ventricular conduction abnormalities, and 8-3-codes as an indication for atrial fibrillation / atrial flutter. After all pairwise tables were summed, the overall agreement, the specific positive and negative agreement were calculated with a 95% confidence interval (CI) for each abnormality. Also, Kappa's with a 95% CI were calculated. The overall agreement (with 95% CI) were for myocardial infarction, ischemic abnormalities, left ventricle hypertrophy, conduction abnormalities and atrial fibrillation/atrial flutter respectively: 0.87 (0.84-0.91), 0.79 (0.74-0.84), 0.81 (0.76-0.85), 0.93 (0.90-0.95), 0.96 (0.93-0.97). This study shows that the overall agreement of the Minnesota code is good to excellent.

Evaluation of risk factors for postoperative ICU admission in a tertiary care hospital – A case control study

Background & objective: Appropriate decisions regarding admission of potential patients to intensive care unit (ICU) postoperatively are considered very important for the patient care. We evaluated the reasons and the risk factors for postoperative ICU admissions in our hospital. Methodology: This is a case-control study, that was done at Security Forces Hospital, Riyadh, during the period from July 2019 to December 2019. We included all patients who needed ICU admission postoperatively in the study as cases. The controls were the patients who had any surgical procedure during the same study period. Patients’ demographics, ASA status, medical co-morbidities and operation details were recorded. We then did univariate and multivariate logistic regression to analyze the data. A p-value of less than 0.05 was considered as significant. Results: We enrolled a total of 140 patients in the study, with 46 cases and 94 controls. In univariate analysis, age, ASA status, presence of hypertension, diabetes, ischemic heart disease, respiratory disease, renal dysfunction and neurological abnormalities were found to be statistically significant predictors for postoperative ICU admission. In multivariate analysis, ASA status and perioperative neurological abnormalities were the most significant risk factors for ICU admission. Conclusion: ASA status and presence of neurological abnormalities are the most significant risk factors associated with ICU admission in the postoperative period. Key words: Risk factors; ICU; ICU admission; Postoperative period; ASA status Citation: Huda AU, Rabbani U, Yasir M. Evaluation of risk factors for postoperative ICU admission in a tertiary care hospital – A case control study. Anesth. pain intensive care 2021;25(4):501–504. DOI: 10.35975/apic.v25i4.1581 Received: December 23, 2020, Reviewed: January 25, 2021, Accepted: July 7, 2021