On Chen

Correlation between pericardial, mediastinal, and intrathoracic fat volumes with the presence and severity of coronary artery disease, metabolic syndrome, and cardiac risk factors

AIMS To investigate the association of pericardial, mediastinal, and intrathoracic fat volumes with the presence and severity of coronary artery disease (CAD), metabolic syndrome (MS), and cardiac risk factors (CRFs). METHODS AND RESULTS Two hundred and sixteen consecutive patients who underwent cardiac magnetic resonance (CMR) imaging and had a coronary angiogram within 12 months of the CMR were studied. Fat volume was measured by drawing region of interest curves, from short-axis cine views from base to apex and from a four-chamber cine view. Pericardial fat, mediastinal fat, intrathoracic fat (addition of pericardial and mediastinal fat volumes), and fat ratio (pericardial fat/mediastinal fat) were analysed for their association with the presence and severity of CAD (determined based on the Duke CAD Jeopardy Score), MS, CRFs, and death or myocardial infarction on follow-up. Pericardial fat volume was significantly greater in patients with CAD when compared with those without CAD [38.3 ± 25.1 vs. 31.9 ± 21.4 cm(3) (P = 0.04)]. A correlation between the severity of CAD and fat volume was found for pericardial fat (β = 1, P < 0.01), mediastinal fat (β = 1, P = 0.03), intrathoracic fat (β = 2, P = 0.01), and fat ratio (β = 0.005, P = 0.01). These correlations persisted for all four thoracic fat measurements even after performing a stepwise linear regression analysis for relevant risk factors. Patients with MS had significantly greater mediastinal and intrathoracic fat volumes when compared with those without MS [126 ± 33.5 vs. 106 ± 30.1 cm(3) (P < 0.01) and 165 ± 54.9 vs. 140 ± 52 cm(3) (P < 0.01), respectively]. However, there was no significant difference in pericardial fat, mediastinal fat, intrathoracic fat, or fat ratio between patients with or without myocardial infarction during the follow-up [33.6 ± 22.1 vs. 35.7 ± 23.8 cm(3) (P = 0.67); 115 ± 26.2 vs. 114 ± 33.8 cm(3) (P = 0.84); 149 ± 44.7 vs. 150 ± 55.7 cm(3) (P = 0.95); and 0.27 ± 0.15 vs. 0.28 ± 0.14 (P = 0.70), respectively]. There was no significant difference in pericardial fat, mediastinal fat, intrathoracic fat, or fat ratio between patients who were alive compared with those who died during follow-up [36.6 ± 26.6 vs. 35.3 ± 23.2 cm(3) (P = 0.76); 114 ± 40.2 vs. 114 ± 31.4 cm(3) (P = 0.95); 150 ± 64.7 vs. 149 ± 52.5 cm(3) (P = 0.92); and 0.29 ± 0.15 vs. 0.28 ± 0.14 (P = 0.85), respectively]. CONCLUSION Our study confirms an association between pericardial fat volume with the presence and severity of CAD. Furthermore, an association between mediastinal and intrathoracic fat volumes with MS was found.

Imaging Modalities to Identity Inflammation in an Atherosclerotic Plaque.

Atherosclerosis is a chronic, progressive, multifocal arterial wall disease caused by local and systemic inflammation responsible for major cardiovascular complications such as myocardial infarction and stroke. With the recent understanding that vulnerable plaque erosion and rupture, with subsequent thrombosis, rather than luminal stenosis, is the underlying cause of acute ischemic events, there has been a shift of focus to understand the mechanisms that make an atherosclerotic plaque unstable or vulnerable to rupture. The presence of inflammation in the atherosclerotic plaque has been considered as one of the initial events which convert a stable plaque into an unstable and vulnerable plaque. This paper systemically reviews the noninvasive and invasive imaging modalities that are currently available to detect this inflammatory process, at least in the intermediate stages, and discusses the ongoing studies that will help us to better understand and identify it at the molecular level.

Echocardiography: a case of coronary sinus endocarditis.

Case: A 23-year-old female with history of hypertension and end-stage renal disease requiring hemodialysis (HD) presented with fever. She had been undergoing HD via a tunneled catheter for a year and presented 3 months prior to this admission for bacteremia with Enterococcus faecalis. At that time she was treated with vancomycin and gentamycin as well as HD catheter replacement and implantation of an arteriovenous (AV) fistula. She was discharged to complete 10 days of intravenous vancomycin during HD and ciprofloxacin orally. She now presented with fever of 102°F during HD, laboratory findings showed a white blood cell count of 30 9 10/L, hemoglobin of 10.2 g/dL, hematocrit of 31%, and platelets of 31 9 10. Basic metabolic panel showed sodium of 134 mEq/L, potassium 5.4 mEq/L, chloride 97 mmol/L, carbon dioxide 25 mmol/L, blood urea nitrogen 81 mg/dL, creatinine 15.1 mg/dL, glucose 203 mg/dL, and calcium 8 mg/dL. Blood cultures were positive for Acinetobacter baumanii. Her fever persisted despite antimicrobial coverage with ampicillin sulbactam and gentamicin intravenously. As her AV fistula was not yet matured a HD catheter was replaced. Transthoracic echocardiogram (Philips iE33, Philips Medical Systems, Andover, MA, USA) performed revealing a mobile structure of 1.4– 0.4 cm in the right atrium, originating from the ostium of the coronary sinus (CS) consistent with vegetation. No valvular involvement was seen (Figs. 1 and 2; Videos S1–S3). With persistent fever and echocardiographic findings, antibiotics were changed from ampicillin sulbactam to meropenem intravenously according to susceptibility. Since the diagnosis of endocarditis was established by echocardiography and her symptoms improved upon treatment of antibiotics, transesophageal echocardiogram was not required. She was discharged with 6 weeks of ceftazidime and gentamicin to be given after dialysis. Her blood cultures turned negative, fever subsided, and her white blood cell count normalized. On outpatient follow-up after completion of antibiotics, the patient had no further febrile events and no further imaging was required. Several months later, the patient underwent removal of her tunneled catheter as her AV fistula was matured for HD access. Address for correspondence and reprint requests: Clara Kwan, M.D., Department of Medicine, Maimonides Medical Center, 4802 Tenth Avenue, Brooklyn, NY 11219. Fax: 718-283-8498; E-mail: clara.kayla@gmail.com Figure 1. An apical four-chamber view with posterior angulation showing a vegetation measuring 1.4 9 0.4 cm is seen in the right atrium, attached to the ostium of the coronary sinus (white arrow) consistent with a vegetation. RA = right atrium; RV = right ventricle; LV = left ventricle.

An avulsed radial artery with a high take-off

A 63-year-old female was diagnosed with severe aortic stenosis, who underwent a diagnostic coronary angiography via transradial approach prior an aortic-valve replacement. After imaging the left coronary system, entrapment of the diagnostic catheter was encountered as a result of spasm of the radial artery. An arteriogram of the arm revealed an anatomical variation in the radial artery (high take-off). Several attempts to remove the entrapped catheter resulted in avulsion of the artery, which was managed successfully with coil embolization. To our knowledge, no such complication has been reported.

Change in P wave morphology after convergent atrial fibrillation ablation.

Convergent atrial fibrillation ablation involves extensive epicardial as well as endocardial ablation of the left atrium. We examined whether it changes the morphology of the surface P wave. We reviewed electrocardiograms of 29 patients who underwent convergent ablation for atrial fibrillation. In leads V1, II and III, we measured P wave duration, area and amplitude before ablation, and at 1, 3 and 6 months from ablation. After ablation, there were no significant changes in P wave amplitude, area, or duration in leads II and III. There was a significant reduction in the area of the terminal negative deflection of the P wave in V1 from 0.38 mm2 to 0.13 mm2 (p = 0.03). There is also an acute increase in the amplitude and duration of the positive component of the P wave in V1 followed by a reduction in both by 6 months. Before ablation, 62.5% of the patients had biphasic P waves in V1. In 6 months, only 39.2% of them had biphasic P waves. Hybrid ablation causes a reduction of the terminal negative deflection of the P wave in V1 as well as temporal changes in the duration and amplitude of the positive component of the P wave in V1. This likely reflects the reduced electrical contribution of the posterior left atrium after ablation as well as anatomical and autonomic remodeling. Recognition of this altered sinus P wave morphology is useful in the diagnosis of atrial arrhythmias in this patient population.

A Rare Case of Renal Infarct due to Noncompaction Cardiomyopathy: A Case Report and Literature Review

Left ventricular noncompaction cardiomyopathy is a rare myocardial disorder which results from failure of left ventricle to compact in embryogenesis. We present a case of a 53-year-old female who came because of abdominal pain and was found to have renal infarct secondary to noncompaction cardiomyopathy.

Asymptomatic giant cardiac fibroma presenting as mitral valve prolapse in an adult patient

A 61 year old woman with a newly diagnosed heart murmur underwent an echocardiogram showing an intramyocardial mass and mitral valve prolapse (Panel A and Panel B). A computed tomography (CT) scan of the chest revealed a round mass in the left chest contiguous with the myocardium of the left lateral wall and no significant mass effect on the cardiac chambers (Panel C). Cardiac magnetic resonance (CMR) revealed a myocardial mass measuring 6 9 5 9 8 cm with well-defined borders beginning at the level of the left atrium, involving the posterior leaflet of the mitral valve and extending to the basal and mid lateral and inferior walls of the left ventricle (Panel D and Panel E). There was no signal enhancement on T2 weighted images (Panel F) and no fat seen on fat saturation sequences (Panel G). The mass appeared to enhance similar to the normal myocardium on first pass perfusion imaging and exhibited marked homogenous delayed Gadolinium enhancement on inversion recovery sequences (Panel H and Panel I). The patient initially underwent an endomyocardial biopsy via right femoral artery under trans-esophageal echocardiogram (TEE) guidance which was unsuccessful, and was later converted to an open thoracoscopic myocardial biopsy. (Panel J). Histological analysis of the biopsied sample revealed bland spindle cells and cardiac myoctes at edge, confirming the diagnosis as cardiac fibroma (Panel K and Panel L) (Fig 1). Cardiac fibromas are rare, benign, intramyocardial tumors that make up 15 % of benign cardiac tumors in children and 3 % of all benign cardiac tumors in adults, with a mean age at presentation of 13 years [1]. Most fibromas originate in the left ventricular free wall or intraventricular septum with symptoms and clinical presentation varying according to the size and the location of the tumor. Common presentations include chest discomfort, syncope, heart failure, cyanosis, arrhythmias or even sudden death but approximately one-third of the patients are asymptomatic and are discovered incidentally on imaging studies [2]. The management of asymptomatic patients, such as our patient is challenging; clinicians have to weigh the risk of surgical resection of the tumor to the benefit of conservative management. In our patient conservative management was elected with close follow-up and referral for evaluation for a heart transplant.

Contralateral embolization of intima after transfemoral aortic valve replacement.

An 88-year-old woman with a history of breast cancer and aortic stenosis presented with heart failure. Echocardiogram showed severe aortic stenosis and valve area of 0.5 cm2. Due to her comorbidities, she was deemed to be at high risk for valve surgery and was evaluated for transcatheter aortic

“Kissing” Vegetation in a Rare Case of Infective Endocarditis by Gemella sanguinis

Infective endocarditis (IE) is usually caused by Streptococcus, Staphylococcus or Enterococcus species or slow-growing HACEK organisms. We report an extremely rare case of IE caused by Gemella sanguinis.

Electrocardiogram in Brugada syndrome

A 35-year-old Chinese male with no past medical history was found unresponsive at home. When emergency medical services arrived at the scene, patient was noted to be in ventricular fibrillation and had to be defibrillated twice. The patient subsequently had a return of spontaneous circulation and was brought to the emergency department (ER). The …