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Background: We have recently shown that PTSD/TBI takes an especially devastating toll on America’s veterans and their families with mental, physical and financial ramifications and poor clinical outcomes (Thakur et al. Epidemiology (Sunnyvale) 2018; 8:353). Patients with PTSD were found to have higher rates of cardiovascular symptoms, hospitalizations and mortality. Whereas electrocardiographic abnormalities, arrhythmias and ventricular dysfunction have been reported in patients with TBI. Association of PTSD/TBI with Myocardial Infarction (MI) is not well studied; the objective of this study was to examine the relationship between PTSD/TBI and MI in a large patient population. Methods: This retrospective study used national data from Veterans Administrations Informatics and Computing Infrastructure (VINCI). Propensity score analysis was performed to obtain matched pairs of (1) Non-PTSD/TBI vs. PTSD (2) Non-PTSD/TBI vs. TBI. Confounding variables used for matching were patients’ demographics and co-morbidities. Cox proportional hazard regression analysis was conducted on matched pairs to determine the relationship between PTSD, TBI and incidence of MI. Kaplan-Meier curves were plotted to compare the time to development of incident MI among the groups. Relationships between variables were examined using chi-square tests, t-tests and non-parametric tests. Results: The risk of new-onset MI was significantly higher for patients with PTSD/TBI when compared with their counterparts without PTSD/TBI. Risk of MI with TBI (HR=2.687, CI 2.546-2.835, P Conclusion: There is a significant increase in the incidence of MI in patients with a diagnosis of PTSD or TBI. Further studies are needed to formulate clinical guidelines to risk stratify and intervene to help reduce the incidence of MI in this patient population.

Background: Multiple observational studies have shown that positive T wave in lead AVR (PTAVR) on 12-lead electrocardiogram is associated with an increased risk of adverse outcomes including death. We sought to review the literature and conduct a meta-analysis to estimate the risk of mortality in patients with PTAVR. Methods: We searched multiple databases to investigate the association between PTAVR and risk of death. Studies that reported adjusted odds ratio (OR) or hazards ratio (HR) of the association between PTAVR and risk of death (all cause or cardiovascular mortality) were included. We used inverse variance approach to pool adjusted OR /HR and it’s 95 % confidence interval using a random effects model meta-analysis. Results: Out of 140 relevant studies, 17 studies were eligible. Twelve studies reported all-cause mortality and enrolled 4,122 patients, 1976 (47.9%) were males. PTAVR was associated with a significant increase in all-cause mortality, with a pooled adjusted OR 2.44, 95% CI [1.76-3.39], heterogeneity I 2 = 86%. Five studies reported cardiovascular mortality and enrolled 31,713 patients, 27,628 (87.1%) were males. PTAVR was associated with a significant increase in cardiovascular mortality, with a pooled adjusted OR 2.34, 95% CI [1.82-3.0], heterogeneity I 2 = 68%. Conclusion: Our findings suggest that PTAVR is significantly associated with a higher risk of death from any cause as well cardiovascular mortality. Lead AVR, an often neglected lead, should be carefully interpreted as it may provide important prognostic information. Further studies are warranted to examined the prognostic value of PTAVR in risk stratification when added to existing cardiovascular risk scores.

Introduction: Improving health status; symptoms, function, and quality of life (QoL) are key treatment goals in patients with peripheral arterial disease (PAD) and claudication. Hypothesis: Compared with medical management only, early revascularization in patients with claudication is associated with greater improvements in disease-specific health status. Methods: Patients with new or worsening claudication, who underwent revascularization within 3 months of enrolment or were treated non-invasively (statin, aspirin, cilostazol, supervised exercise therapy, risk factor management) were identified from 16 vascular medicine clinics in the US, Netherlands and Australia participating in the PORTRAITregistry. Patients were propensity-matched on the likelihood of receiving invasive therapy. The Peripheral Artery Questionnaire (PAQ) was used to assess patients’ disease-specific health status at enrollment, and at 3, 6 and 12 months of follow-up using hierarchical Generalized Linear Models for repeated measures. Results: Among 1142 patients (mean age of 67.7 years, 63.0% male), 229 (20.1%) underwent early revascularization while 913 (79.9%) were managed non-invasively. At baseline, patients who underwent invasive vs. non-invasive management had lower PAQ summary (mean ± SD; 44.41 ± 19.98 vs 50.98 ± 21.79, PFigure 1 ). Conclusion: Patients who underwent early revascularization had worse baseline health status but a greater improvement over 1 year of follow-up when compared with patients managed without revascularization. Summarizing real-world health status benefits following a PAD diagnosis can support preference-sensitive decisions for PAD management.

Ascending (type A) aortic dissection can rarely result in contained transverse pericardial sinus hematoma that compresses adjacent structures making diagnosis more challenging. We present a rare case of a 77-year-old man who presented with sudden-onset chest pain and was admitted for a presumed acute coronary syndrome. Coronary angiography did not show significant stenosis and ruled out acute coronary syndrome. Transthoracic echocardiogram showed extracardiac structure compressing on the left atrium; hence, we performed transesophageal echocardiogram which confirmed aortic dissection and revealed a hematoma in the transverse pericardial sinus. Intraoperatively, a large hematoma in the transverse pericardial sinus was extracted and revealed a posterior perforation of the ascending aorta that extended into the left atrium.

Three cases from 2 institutions are presented in which patients developed asystole and/or severe bradycardia following the use of regadenoson for myocardial perfusion imaging (MPI), potential causes are posited, and directed therapy is suggested. The first case is that of an 81-year-old man with

Introduction. Streptococcal pharyngitis has been historically complicated with systemic involvement manifesting as acute rheumatic fever, which is a serious condition that can lead to permanent damage to heart valves. A recent association between streptococcal pharyngitis and nonrheumatic heart disease is emerging in literature. We present a case of nonrheumatic streptococcal myocarditis diagnosed using cardiac MRI. Case Presentation. A 25-year-old male, presented with complaints of sore throat, nonproductive cough, fever, pleuritic chest pain, and progressive dyspnea for four days. The patient had elevated troponins at presentation of 0.47 (ng/L) that peaked at 4.0 (ng/L). ECG showed sinus rhythm and ST elevations in leads V2, V3, V4, and V5. NT-Pro-BNP was 1740. Transthoracic echocardiogram (TTE) showed reduced ejection fraction (EF) of 37% and global hypokinesis. The rapid strep test was positive for group A streptococcus and C-reactive protein was elevated at 161. Cardiac MRI demonstrated an EF of 53% and edema in the anterior wall without delayed gadolinium enhancement. Cardiac catheterization showed normal coronaries. Discussion. According to modified Jones criteria, the patient did not meet the full major or minor criteria to be diagnosed with acute rheumatic fever. The course of the nonrheumatic myocarditis is favorable and includes a full recovery of cardiac function, no involvement of cardiac valves, or long-term use of antibiotics. Conclusion. It is crucial to make a separate distinction between acute rheumatic fever and nonrheumatic myocarditis because this will have huge implications on management and long-term use of antibiotics. Cardiac imaging modalities can aid in distinction between the two disease entities.

We present a rare case of rasburicase-induced methemoglobinemia and hemolytic anemia in the setting of presumed glucose-6-phosphate dehydrogenase (G6PD) deficiency. A 78-year-old male with a known history of chronic lymphocytic leukemia presented to the clinic with fever of unknown origin. Laboratory results were significant for hyperuricemia. He was empirically started on levofloxacin and rasburicase. He then presented to the emergency department with shortness of breath and syncope. Physical examination was remarkable for a fever of 102.8 °F, conjunctival pallor, and scleral icterus. An infiltrate was observed on his computed tomography (CT) angiogram of the chest. Arterial blood gas on 50% fraction of inspired oxygen was significant for an arterial oxygen level of 222 millimeters mercury and oxyhemoglobin of 85.9%. Co-oximetry was then obtained and methemoglobin level was 13.4%. Laboratory results were noteworthy for a drop-in hemoglobin, indirect hyperbilirubinemia, low haptoglobin and elevated lactate dehydrogenase; depicting hemolytic anemia. The patient received two units of packed red blood cells, intravenous broad-spectrum antibiotics and he clinically improved.

Physiologic parameters quantified by positron emission tomography (PET) myocardial perfusion imaging (MPI), such as coronary flow reserve (CFR) and left ventricular ejection fraction reserve (LVEFr), improve identification of patients with obstructive 3-vessel or left main (3VD/LM) coronary artery

A 78-year-old man was referred from his primary care clinic to the emergency department due to bluish discolouration of his lips and decreased oxygen saturation on pulse oximetry. The patient was asymptomatic. Physical exam was normal except for lip cyanosis. A CT pulmonary angiogram was negative for pulmonary embolism. Arterial blood gas (ABG) analysis with co-oximetry showed low oxyhaemoglobin, normal partial pressure of oxygen and methaemoglobinaemia, but an unexplained ‘gap’ in total haemoglobin saturation. This gap was felt to be due to sulfhaemoglobinaemia. After a thorough review of his medications, ferrous sulfate was stopped which resulted in resolution in patient’s cyanosis and normalisation of his ABG after 7 weeks.