Anwer Qureshi

Clinical Significance of Epicardial Fat Measured Using Cardiac Multislice Computed Tomography

Cardiac adiposity defined as increased epicardial adipose tissue and massive deposits of fat within the atrial septum (lipomatous hypertrophy) is seen in overweight persons and is associated with coronary artery disease (CAD), atrial arrhythmias, and increased risk of left ventricular free wall rupture after acute myocardial infarction. Unlike subcutaneous fat, epicardial fat is metabollically active and produces hormones, cytokines, and other vasoactive substances that work systemically or locally to alter vascular endothelial function and may be implicated in the pathogenesis of CAD. The aim of the study was to assess the feasibility of measuring epicardial fat volume (EFV) and identify its clinical correlates using (64-slice) multislice computed tomography (MSCT). A protocol was devised to measure EFV using MSCT in 151 adults (age 26 to 83 years, mean 51 +/- 12; 55% men). Cross-sectional tomographic cardiac slices (2.5-mm thick) from base to apex (range 28 to 40 per heart) were traced semiautomatically using an off-line workstation, and EFV was measured by assigning Hounsfield units ranging from -30 to -250 to fat. Coronary computed tomographic angiography was performed using a standard protocol. EFV ranged from 25 to 274 ml (mean 121 +/- 47), corresponding to 2.4% to 30.5% (mean 15 +/- 5%) of total cardiac volume and correlated with age, atrial septum thickness, body weight, and body mass index. Coronary calcium score was significantly higher in patients with EFV >100 ml (67 +/- 155 vs 216 +/- 639; p = 0.03), and a higher percentage of patients with increased EFV had CAD (46% vs 31%; p <0.05) or metabolic syndrome (44% vs 29%; p <0.05). In conclusion, quantification of EFV was feasible using MSCT. Large deposits of fat around the heart and within the atrial septum were associated with obesity, coronary calcium, metabolic syndrome, and CAD. Measurement of EFV may provide another useful noninvasive indicator of heightened risk of CAD in addition to calcium score and coronary angiography.

Novel variant of dual left anterior descending coronary artery

A 29-year-old African American man presented with atypical chest pain. Coronary computed tomographic angiography (64-slice) showed a previously not described variant of dual (duplicated) left anterior descending artery (LAD). Duplication of LAD is a rare anomaly and has been categorized into 4 angiographic subtypes based on the origin, course, and termination of the short and long LAD. Our case is unique in that, unlike previous subtypes, the short LAD originates independently from the left coronary sinus and that the long LAD arises from the right coronary sinus and has an intramyocardial course before reaching the distal interventricular groove. It can be, thus, considered a new variant of dual LAD (type V).

Echocardiographic guidance in treatment of cardiogenic shock complicating transient left ventricular apical ballooning syndrome.

TRANSIENT LEFT VENTRICULAR APICAL BALLOONING (TLVAB) SYNDROME can rarely present with cardiogenic shock ([1][1]). While a cardiogenic shock like picture is likely due to left ventricular systolic dysfunction, dynamic midventricular or left ventricular outflow tract (LVOT) obstruction can occur and

Simultaneous massive pulmonary embolism and impending paradoxical embolism through a patent foramen ovale.

![Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4][![Graphic][5] ][5] A 66-year-old obese woman presented with shortness of breath over 8 weeks. She was hemodynamically stable. D-dimer was elevated at 2.14. Transthoracic (Online Video [1][5]) followed by transesophageal

Possible Link Between Apical Ballooning Syndrome During Anaphylaxis and Inappropriate Administration of Epinephrine–1

We read with interest the letter by Manivannan et al describing a patient with ABS due to intravenous epinephrine injection given for anaphylactic reaction after a bee sting. We would like to broaden the differential diagnosis in a scenario such as this. Acute coronary syndrome during an anaphylactic reaction, especially in those who receive epinephrine, can occur for a variety of reasons, including (1) ABS or stress cardiomyopathy, (2) allergic myocardial infarction (ie, Kounis syndrome [KS]), and (3) hypersensitive myocarditis (HM). Apical ballooning syndrome affects mainly women during emotional stress and is characterized by the presence of normal coronary arteries and reversible apical ventricular dysfunction. In this syndrome, it is thought that myocardial stunning occurs as a result of high levels of circulating (ie, endogenous) catecholamines. Epinephrine triggers a switch in intracellular signal trafficking in ventricular cardiomyocytes from Gs protein to Gi protein signaling via the β2-adrenoceptor, which in turn protects against the proapoptotic effects of the intense activation of β1-adrenoceptors. However, this change also causes a negative inotropic effect. Because β-adrenoceptor density is greatest at the apical myocardium, this effect is greatest in that region. Other mechanisms have also been implicated. It is not surprising that a supratherapeutic dose of intravenous epinephrine could produce a similar phenomenon, as postulated by Manivannan et al. However, this is not the first reported case of ABS due to the administration of epinephrine, as the authors claim. Six cases of stress cardiomyopathy due to epinephrine and 3 due to dobutamine were recently described by Abraham et al.1 The dose of epinephrine ranged from a minimum of 1 mg to 40 mg. Some recent reports have even linked this syndrome to anaphylactic reaction.2 However, other possible etiologies of ABS after a bee sting must also be entertained. The coincidental occurrence of chest pain, electrocardiographic changes, and elevated troponin levels during anaphylactic reaction to bee sting has previously been described as KS by various authors.3 During hypersensitive reactions, sudden release of histamine and other inflammatory mediators from mast cells, macrophages, and T lymphocytes has been postulated to lead to coronary vasospasm and hence to acute coronary syndrome. A myocardial biopsy will reveal a normal myocardium. However, KS may occur in association with ABS because various cytokines have been implicated in the causation of ABS. In this context, exogenous administration of epinephrine is not required for the development of ABS. A case report of KS with ABS has been published.4 Hypersensitive reactions may also involve the heart by causing HM. In patients with HM, the myocardial biopsy will reveal the presence of eosinophils, atypical lymphocytes, and giant cells. Clinically, it is difficult to differentiate HM from KS because both present with signs and symptoms of acute coronary syndrome and for both coronary angiography reveals normal coronary arteries. The patient described by Manivannan et al had ventricular dysfunction typical of ABS in the presence of an anaphylactic reaction. Hence, we propose that she had KS complicated by ABS due to epinephrine and release of cytokines from the allergic reaction to the bee sting. As such, exogenous epinephrine administration need not be credited as the sole origin of ABS in this patient.

Impact of Clinical Predictors and Routine Coronary Artery Disease Testing on Outcome of Patients Admitted to Chest Pain Decision Unit

Chest pain decision unit (CDU) evaluation of patients with acute chest pain (ACP) and nondiagnostic electrocardiogram (ECG) usually includes noninvasive testing for coronary artery disease (CAD).

Apicoaortic Double-Valved Conduit in a 40-Year-Old Woman

A 40-year-old woman was admitted with pneumonia and septic shock. Chest x-ray showed bilateral pulmonary infiltrates, cardiomegaly, and a bioprosthetic valve in an unusual position near the left ventricular apex (Figure 1A). The patient had a history of muscular subaortic stenosis. At age 4, she underwent surgical resection, but severe subaortic stenosis recurred 5 years later when an apicoaortic conduit containing an Ionescu–Shiley bioprosthetic valve was placed between the left ventricular apex and the descending thoracic aorta. Six …