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The American Journal of the Medical Sciences | 2009

Reduced Relative Lymphocyte Count in African-Americans With Decompensated Heart Failure

Sheharyar Ali; Atta U. Shahbaz; Maeda D. Nelson; Karl T. Weber; Arsalan Shirwany; Ahmad Munir; Ivan C. D’cruz

Background:A reduction in relative lymphocyte count (%L) has been reported in whites with heart failure that inversely correlated with jugular venous pressure thereby implicating systemic venous hypertension with splanchnic congestion. Objectives:To study whether a reduced %L (<20%) occurs in African-Americans (AA) with heart failure and to address pathophysiologic mechanisms having the potential to influence lymphocyte biology and survival, we monitored patients with or without systemic venous hypertension, hypoalbuminemia, hypovitaminosis D, and secondary hyperparathyroidism. Methods:In 131 AA (90 men; 53 ± 12 years): 113 were hospitalized, 50 with decompensated biventricular failure (DecompHF), 24 with acute left heart failure, and 39 with heart disease, but no heart failure (HDNHF); and 18 were outpatients with compensated heart failure. At the time of admission or outpatient visit, we monitored: white blood cell count and %L; and serum albumin, 25(OH)D, and parathyroid hormone (PTH). Results:White blood cell count did not differ among the groups, whereas %L was reduced only in those with DecompHF (15 ± 1%; P < 0.05) versus 25 ± 2% with left heart failure, 29 ± 1% in HDNHF, and 28 ± 3% in compensated heart failure. Serum albumin was reduced in DecompHF (2.8 ± 0.1; P < 0.05), but not in any of the other groups. Reduced 25(OH)D (<30 ng/mL), in keeping with hypovitaminosis D, was found in all AA, whereas elevated serum PTH (>65 pg/mL) was found only in those with DecompHF (123 ± 22 pg/mL). Conclusions:A relative lymphocytopenia, together with hypoalbuminemia and elevated PTH, were found only in hospitalized AA with DecompHF. These findings implicate splanchnic congestion and the enteric loss of lymphocytes and albumin with an associated secondary hyperparathyroidism.


Echocardiography-a Journal of Cardiovascular Ultrasound and Allied Techniques | 2004

Posterior Mediastinal Spread of Bronchogenic Carcinoma Simulating a Mass Within the Left Atrium

Paulo Cesar Campos; Ivan A. D'Cruz; Husni W. Dweik; Arsalan Shirwany; Monica Umpierrez

(ECHOCARDIOGRAPHY, Volume 21, May 2004)


Canadian Journal of Cardiology | 2008

Vasospasm-induced polymorphic ventricular tachycardia

Saurabh S. Dhawan; Arsalan Shirwany

A 63-year-old man was admitted for workup of syncope and episodic, midsternal chest pain of one-year duration. During another episode of chest pain after admission, the electrocardiogram (Figure 1) revealed a heart rate of 55 beats/min; ST elevation in leads II, III and aVF; with reciprocal ST depression in leads I and aVL and upsloping ST depression in leads V1 to V4, demonstrating inferior and posterior wall myocardial ischemia. The telemetry rhythm strip (Figure 2) revealed ST elevation followed by wide-complex polymorphic ventricular tachycardia at 300 beats/min, characteristic of torsades de pointes that resolved 5 min later. Cardiac enzymes were within normal limits. Transthoracic echocardiography showed no ventricular dysfunction or wall motion abnormalities and cardiac catheterization revealed no evidence of stenotic coronary artery disease. These findings demonstrate polymorphic ventricular tachycardia in the setting of variant or Prinzmetal’s angina in the absence of obstructive coronary artery disease (1). The patient was subsequently treated with felodipine and a nitroglycerin patch to prevent episodes of variant angina, and reported no further episodes in six months of follow-up (2). Figure 1) Electrocardiogram revealing a heart rate of 55 beats/min; ST elevation in leads II, III and aVF, with reciprocal ST depression in leads I and aVL and upsloping ST depression in leads V1 to V4, demonstrating inferior and posterior wall myocardial ischemia ... Figure 2) Telemetry rhythm strips revealing ST elevation followed by wide-complex polymorphic ventricular tachycardia at 300 beats/min, characteristic of torsades de pointes that resolved 5 min later. Strip 1 Vasospasm; Strip 2 Polymorphism; Strip 3 Normal sinus ...


Canadian Journal of Cardiology | 2008

Automatic implantable cardioverter defibrillator pocket infection leading to extrusion of the generator device

Saurabh S. Dhawan; Shadwan Alsafwah; Arsalan Shirwany

A 52-year-old man with dilated cardiomyopathy underwent automatic implantable cardioverter defibrillator (AICD) placement. A follow-up visit eight weeks later revealed erythema of the implant site, but expectant management was pursued. Six months later, increasing redness, pain and extrusion of the generator device that morning on local treatment with hydrogen peroxide brought the patient to the hospital. A physical examination demonstrated no fever, a wound in the left upper chest with the extruded AICD battery, erythema and tenderness (Figure 1). Bacterial culture grew methicillin-resistant Staphylococcus epidermidis. The patient subsequently underwent treatment with intravenous antibiotics and a complete AICD explantation (1). Figure 1) Photograph depicting an extruded automated cardioverter defibrillator battery covered with yellow crust, physcially intact leads, erythema and swelling of the surrounding area. The original incision made in the deltopectoral groove at the time of automated ...


Journal of Investigative Medicine | 2006

46 CAN THE RIGHT SUBCLAVIAN VEIN BE USED AS A SURROGATE OF THE INFERIOR VENA CAVA AS AN INDICATOR OF SYSTEMIC VENOUS CONGESTION?: Table

Ahmad Munir; Arsalan Shirwany; Ivan A. D'Cruz; Daniel Minderman

Background The respiratory variation (RV) in inferior vena cava (IVC) caliber is routinely evaluated on echo for assessment of systemic venous congestion. In obese patients or in those who have recently undergone abdominal or thoracic surgery, IVC visualization can be difficult. We assessed whether RV in the right subclavian vein (RSV) caliber can serve as a surrogate for the RV in the IVC and whether the correlation would be better with the imaging performed in supine position or at a 458 reclining position. Methods In 40 patients, IVC long axis echocardiograms were recorded for 10 beats with patient breathing normally. M-mode recordings were made of the IVC segment 2 to 4 cm inferior to the entry of the IVC into the right atrium, and the minimum (MIN) and maximum (MAX) IVC diameters were obtained. RSV was visualized from the right supraclavicular region. Two-dimensional recordings were made over 10 beats during normal quiet respiration in the supine and in the 458 reclining position; MIN and MAX diameters were obtained and ratio calculated. Correlation between ratio of the MIN to MAX IVC caliber and ratio of RSV MIN to MAX caliber was tested by statistical analysis. Results The mean ratio of respiratory variation of IVC caliber was different from the mean ratio of the respiratory variation in the RSV in the supine position but not from the mean ratio of the respiratory caliber variation in the RSV at 458 position. Using the paired t-test, the IVC respiratory variation correlated better with the RSV respiratory variation in the 458 reclining position. Table Minimum/Maximum Diameter Ratio Conclusions Respiratory variation in RSV caliber at 458 correlates well with the IVC respiratory variation and can be used for noninvasive assessment of systemic venous congestion if the IVC cannot be visualized well due to obesity, recent surgery, or other reasons.


Echocardiography-a Journal of Cardiovascular Ultrasound and Allied Techniques | 2004

Pectus Excavatum Associated with Pulmonary Artery Dilatation

Ivan A. D'Cruz; Arsalan Shirwany; Paul Gerlach

Pectus excavatum is the commonest congenital deformity of the anterior chest wall. We describe a case of dilatation of the pulmonary trunk and proximal right and left main pulmonary arteries, associated with pectus excavatum obstructing the right ventricular outflow, the first such case to the best of our knowledge. The patient was a small thin 63-year-old man admitted with the acute onset of leftsided weakness. Three weeks earlier, he had been hospitalized and treated for mycobacterium avium-intercellulare pneumonia. Chest examination revealed conspicuous pectus excavatum and a systolic murmur along the left sternal border. He manifested a left hemiplegia and slurred speech. No features of Marfan syndrome were noted. Chest X-ray showed bilateral lung infiltrates, and a prominent bulge on the upper left border of the cardiac silhouette corresponding to the pulmonary artery. CT scan of the thorax showed dilatation of the pulmonary trunk and right pulmonary artery, and encroachment of the pectus excavatum deformity on the right ventricular outflow tract (Fig. 1). Transthoracic echocardiography revealed marked dilatation of the pulmonary trunk, but satisfactory images of most cardiac structures could not be obtained due to poor acoustic windows. Transesophageal echocardiography was then performed (Figs. 2 and 3). The left ventricular size and systolic function and all the valves, including the pulmonic valve, ap-


Journal of the American College of Cardiology | 2006

Extracellular Matrix Remodeling in Hypertensive Heart Disease

Arsalan Shirwany; Karl T. Weber


The American Journal of Medicine | 1999

Infectious aortitis : An uncommon manifestation of infection with Streptococcus pneumoniae

Michael S. Bronze; Arsalan Shirwany; Cathy E. Corbett; Dennis Schaberg


Clinical Infectious Diseases | 1998

Urinary tract aspergillosis in a renal transplant recipient.

Arsalan Shirwany; Susie Sargent; Roger R. Dmochowski; Michael S. Bronze


Journal of the American College of Cardiology | 2006

Extracellular Matrix Remodeling in Hypertensive Heart Disease* * Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology

Arsalan Shirwany; Karl T. Weber

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Ivan A. D'Cruz

University of Tennessee Health Science Center

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Karl T. Weber

University of Tennessee Health Science Center

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Ahmad Munir

University of Tennessee Health Science Center

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Michael S. Bronze

University of Oklahoma Health Sciences Center

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Atta U. Shahbaz

University of Tennessee Health Science Center

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Cathy E. Corbett

University of Tennessee Health Science Center

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Daniel Minderman

University of Tennessee Health Science Center

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Dennis Schaberg

University of Tennessee Health Science Center

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Husni W. Dweik

University of Tennessee Health Science Center

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