Obstructive apneas produce high negative intrathoracic pressure that imposes an afterload burden on the left ventricle. Such episodes might produce structural changes in the left ventricle over time. Doppler echocardiograms were obtained within 2 months of attended polysomnography. Patients were grouped according to apnea-hypopnea index (AHI): mild/no obstructive sleep apnea (OSA; AHI <15) and moderate/severe OSA (AHI >= 15). Mitral valve tenting height and area, left ventricular (LV) long and short axes, and LV end-diastolic volume were measured in addition to tissue Doppler parameters. Comparisons of measurements at baseline and follow-up between and within groups were obtained; correlations between absolute changes (Delta) in echocardiographic parameters were also performed. After a mean follow-up of 240 days mitral valve tenting height increased significantly (1.17 +/- 0.12 to 1.28 +/- 0.17 cm, p = 0.001) in moderate/severe OSA as did tenting area (2.30 +/- 0.41 to 2.66 +/- 0.60 cm(2), p = 0.0002); Delta tenting height correlated with Delta LV end-diastolic volume (rho 0.43, p = 0.01) and Delta tenting area (rho 0.35, p = 0.04). In patients with mild/no OSA there was no significant change in tenting height; there was a borderline significant increase in tenting area (2.20 +/- 0.44 to 2.31 +/- 0.43 cm(2), p = 0.05). Septal tissue Doppler early diastolic wave decreased (8.04 +/- 2.49 to 7.10 +/- 1.83 cm/s, p = 0.005) in subjects with moderate/severe OSA but not in in those with mild/no OSA. In conclusion, in patients with moderate/severe OSA, mitral valve tenting height and tenting area increase significantly over time. This appears to be related, at least in part, to changes in LV geometry. (C) 2012 Elsevier Inc. All rights reserved. (Am J Cardiol 2012;109: 1055-1059)

BACKGROUND:Saddle pulmonary embolism represents a large clot and a risk for sudden hemodynamic collapse. However, the clinical presentation and outcomes vary widely. On the basis of the findings of right heart dysfunction on echocardiograms, computed tomography angiography, or cardiac enzyme elevation, some argue for the use of thrombolytics or catheter thrombectomy even for hemodynamically stable patients.OBJECTIVE:To investigate the outcomes and management of patients with saddle pulmonary embolism, including radiographic appearance (estimate of clot burden) and echocardiographic features.INTERVENTIONS:None.MEASUREMENTS AND MAIN RESULTS:This study is a retrospective evaluation of all patients with computed tomography angiography positive for pulmonary embolism from June 1, 2004, to February 28, 2009. Two radiologists selected those with saddle pulmonary embolism and evaluated the clot burden score. The clinical information, echocardiography, treatments, and outcomes of these patients were extracted via chart review. Saddle pulmonary embolism was found in 37 of 680 patients (5.4%, 95% confidence interval 4% to 7%) with documented pulmonary embolism on computed tomography angiography. For patients with saddle pulmonary embolism, the median age was 60 yrs and 41% were males. Major comorbidities were neurologic (24%), recent surgery (24%), and malignancy (22%). Transient hypotension occurred in 14% and persistent shock in 8%. One patient required mechanical ventilation. Echocardiography was performed in 27 patients (73%). Right ventricle enlargement and dysfunction were found in 78% and elevated pulmonary artery systolic pressure in 67%. Computed tomography angiography demonstrated a high median pulmonary artery clot burden score of 31 points. The median right ventricle to left ventricle diameter ratio was 1.39. Inferior vena cava filters were placed in 46%. Unfractionated heparin was administered in 33 (87%) and thrombolytics in four (11%). The median hospital length of stay was 9 days. Two of 37 saddle pulmonary embolism patients (5.4%) died in the hospital (95% confidence interval 0.7% to 18%).CONCLUSIONS:Most patients with saddle pulmonary embolism found on computed tomography angiography responded to the standard management for pulmonary embolism with unfractionated heparin. Although ominous in appearance, most patients with saddle pulmonary embolism are hemodynamically stable and do not require thrombolytic therapy or other interventions.

Introduction: It is known that with increasing age impaired myocardial relaxation increases, while systolic function is preserved. We hypothesize that there is, in fact, subclinical left ventricular (LV) systolic dysfunction in older subjects. We test this hypothesis by assessing LV systolic strain using velocity vector imaging in older subjects with no known cardiac disease. Methods: One-hundred and ninety consecutive subjects with no known cardiac disease had their echocardiograms analyzed by VVI after excluding patients with a left ventricular ejection fraction(LVEF) <55%, grade 2 and above diastolic dysfunction and QRS duration > 120ms. Subjects were divided into 2 groups based on age; older (> 60 years) and younger (< 60 years). Demographic, clinical and echocardiographic data were collected. Time to peak longitudinal and circumferential strain were calculated from apical 4-chamber, 2-chamber and short axis views. The above collected data were compared between groups. Results: The final cohort consisted of 136 subjects (46 were older). Mean age was 55 + 16 years, 32% were female and mean LVEF was 60 + 8%. The older group had a higher LVEF (63 + 9% vs. 59 + 6%; p=0.03), smaller LV diastolic dimension (4.4 + 0.5cm vs. 4.7 + 0.5cm; p<0.01) and higher occurrences of diastolic dysfunction (84% vs. 59%; p<0.01) and hypertension (85% vs. 63%; p=0.02), when compared to the younger group. There were no significant differences in the longitudinal and circumferential strain (even with cut-off ages of 50 or 75 years). Conclusions: Contrary to our hypothesis, older subjects with no known cardiac disease had a better LVEF than their younger counterparts. There were no significant differences in the longitudinal and circumferential myocardial strain between the older and younger groups. Therefore, impaired myocardial relaxation does not appear to have a direct influence on the myocardial contractility or systolic function in older subjects.

Left ventricular outpouchings are increasingly detected on cardiovascular imaging. Herein, we describe the case of a 45-year-old man who underwent noncardiac preoperative imaging and was found to have an asymptomatic left ventricular outpouching. The patient underwent successful surgical repair of the structure. When left ventricular outpouchings are detected, the main differential diagnoses are pseudoaneurysm, aneurysm, and diverticulum. The outcomes for these conditions differ substantially, and accurate diagnosis can be crucial in making clinical decisions. We review the relevant medical literature, outline the natural history of these left ventricular abnormalities, and discuss options in regard to their management.

OBJECTIVE The study was undertaken to assess the correlation between the presence and degree of aortic atheroma with degree of Left ventricular (LV) mass index and subsequent clinical outcomes. MATERIAL AND METHOD The authors studied the clinical profiles of 87 patients with aortic atherosclerosis and controls, who had undergone TEE between 1995 and 2000. RESULTS Mean LV mass index was 116 gram/m2 in atherosclerosis group compared to 81 gram/m2 in the control group (p < 0.009). In the atherosclerotic group, there was a close correlation between LV mass index score and severity of the plaque in the aortic arch and descending aorta (p < 0.001, 0.001). The presence of large ulcerated plaque had a significant correlation with stroke (p < 0.002). CONCLUSION 1) LV mass index correlates with the severity of aortic atheroma. 2) Smoking, elevated mean arterial blood pressure and a high LV mass index score are significantly correlated with large ulcerated plaque and stroke. 3) These findings may in part explain the higher cardiovascular risk in patients with increased left ventricular mass.

Background: Dobutamine stress echocardiography (DSE) is frequently used in the evaluation of cardiac risk prior to orthotopic liver transplantation (OLT). In the general cardiac population, an inducible left ventricular outflow tract gradient (LVOT Δ) during DSE has variable prognostic importance. The purpose of this study was to determine the prevalence and clinical significance of LVOT Δ in patients undergoing OLT during DSE. Methods: Consecutive medical records of 106 patients who had undergone OLT at our institution from January 1997 until January 2002 were retrospectively analyzed and divided into two groups based on the presence (Group I, LVOT Δ > 36 mmHg) or absence (Group II, LVOT Δ≤ 36 mmHg) of a significant LVOT Δ measured during DSE. We determined any outcome differences between these two groups with regard to intraoperative hypotension, cardiac mortality, length of hospital stay, graft function, and renal function post‐OLT. Results: Forty‐six patients had an LVOT Δ > 36 mmHg (Group I) and 60 patients had LVOT Δ≤ 36 mmHg (Group II). Baseline demographics were similar in both groups. There was no significant overall difference in cardiac mortality between Group I versus Group II patients (0 versus 1 patient, respectively, P = 0.57). Intraoperative hypotension occurred in 4 patients in Group I versus 0 patient in Group II (P = 0.03). Length of stay, graft function, and postoperative renal function were similar in both groups. Conclusion: A significant LVOT Δ > 36 mmHg is a frequent finding occurring in 46/106 (43%) of patients who have DSE pre‐OLT. Intraoperative hypotension is associated with patients having an LVOT Δ. However, post‐OLT patients with significant LVOT Δ have a similar in‐hospital outcome compared to patients without significant LVOT Δ.

EchocardiographyVolume 20, Issue 6 p. 557-559 Resolution of a Primary Intracardiac Lymphoma Suraj Maraj , M.D., Suraj Maraj , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorRichard G. To , M.D., Richard G. To , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorGuillermo Crespo , M.D., Guillermo Crespo , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs , M.D., Larry E. Jacobs , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler , M.D., Morris N. Kotler , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this author Suraj Maraj , M.D., Suraj Maraj , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorRichard G. To , M.D., Richard G. To , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorGuillermo Crespo , M.D., Guillermo Crespo , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs , M.D., Larry E. Jacobs , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler , M.D., Morris N. Kotler , M.D. Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Jefferson University School of Medicine, Philadelphia, PennsylvaniaSearch for more papers by this author First published: 14 July 2003 https://doi.org/10.1046/j.1540-8175.2003.03094.x Address for correspondence and reprint requests: Morris N. Kotler, M.D., Albert Einstein Medical Center, 363 Klein Professional Building, 5401 Old York Road, Philadelphia, PA 19141. Fax: (215) 455-6189; E-mail: [email protected] Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 McCallister HA, Fenoglio JJ: Tumors of the cardiovascular system. In: Atlas of Tumor Pathology (2nd Series, Fasicle 15). Washington , DC : Armed Forces Institute of Pathology , 1978, pp. 99–100. 2 Nand S, Mullen GM, Lonchyna VA, et al: Primary lymphoma of the heart. Cancer 1991; 68: 2289–2292. Volume20, Issue6August 2003Pages 557-559 ReferencesRelatedInformation

A right ventricular thrombus (RVT) is an unusual finding on echocardiography. We describe a healthy young male patient who developed RVT with subsequent pulmonary embolism (PE), the etiology of which remains uncertain. (ECHOCARDIOGRAPHY, Volume 20, July 2003)

EchocardiographyVolume 20, Issue 8 p. 737-738 Aortoventricular Fistula and Abscess Caused by Vancomycin-Resistant Enterococcus in a Hemodialysis Patient Suraj Maraj M.D., Suraj Maraj M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs M.D., Larry E. Jacobs M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorEnakshi Bajpai D.O., Enakshi Bajpai D.O. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorGuillermo Crespo M.D., Guillermo Crespo M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler M.D., Morris N. Kotler M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this author Suraj Maraj M.D., Suraj Maraj M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs M.D., Larry E. Jacobs M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorEnakshi Bajpai D.O., Enakshi Bajpai D.O. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorGuillermo Crespo M.D., Guillermo Crespo M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler M.D., Morris N. Kotler M.D. Echocardiography Laboratory, Division of Cardiology, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this author First published: 01 December 2003 https://doi.org/10.1111/j.0742-2822.2003.02142.x Address for correspondence and reprint requests: Larry E. Jacobs, M.D., Albert Einstein Medical Center, 363 Klein Professional Building, 5401 Old York Road, Philadelphia, PA 19141; Fax: (215) 456-6189; E-mail: [email protected] Supported in part by The Women's League for Medical Research, Albert Einstein Medical Center. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Samuels LE, Kaufman MS, Rodriguez-Vega J, et al: Diagnosis and management of traumatic aorto-ventricular fistulas. Ann Thorac Surg 1998; 65: 288– 292. 2 Roy D, Saba S, Grinberg I, et al: Aorto-right ventricular fistula: A late complication of aortic valve replacement. Tx Heart Inst J 1999; 26: 140– 142. 3 Mizock BA, Nachman SA, Varquez M: Left ventricular outflow tract pulmonary artery fistula in endocarditis. Clin Cardiol 1995; 18: 539– 540. 4 Elian D, Di Segni E, Kaplinsky E, et al: Acquired left ventricular-right atrial communication caused by infective endocarditis detected by transesophageal echocardiography: Case report and review of the literature. J Am Soc Echocardiogr 1995; 8: 108– 110. Volume20, Issue8November 2003Pages 737-738 ReferencesRelatedInformation

Penetrating aortic atherosclerotic ulcers have been recently recognized as an entity among the acute aortic syndromes with a potentially fatal outcome. We describe the case of a patient presenting with severe chest pain who died as a result of a thoracic-aorta penetrating atherosclerotic ulcer complicated by a intramural hematoma of the esophagus and stomach, leading to exsanguination. To our knowledge this is the first case reported in the literature of such a complication from penetrating aortic atherosclerotic ulcers.

EchocardiographyVolume 20, Issue 2 p. 199-200 Cisplatin Induced Localized Aortic Thrombus Sirin Apiyasawat M.D., Sirin Apiyasawat M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorNattawut Wongpraparut M.D., Nattawut Wongpraparut M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLaura Jacobson M.D., Laura Jacobson M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorHenry Berkowitz M.D., Henry Berkowitz M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs M.D., Larry E. Jacobs M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler M.D., Morris N. Kotler M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this author Sirin Apiyasawat M.D., Sirin Apiyasawat M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorNattawut Wongpraparut M.D., Nattawut Wongpraparut M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLaura Jacobson M.D., Laura Jacobson M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorHenry Berkowitz M.D., Henry Berkowitz M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs M.D., Larry E. Jacobs M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler M.D., Morris N. Kotler M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this author First published: 10 March 2003 https://doi.org/10.1046/j.1540-8175.2003.03002.xCitations: 16 Address for correspondence and reprint requests: Morris N. Kotler, M.D., Albert Einstein Medical Center, 363 Klein Professional Building, 5401 Old York Road, Philadelphia, PA 19141. Fax: 215-456-6189. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume20, Issue2February 2003Pages 199-200 RelatedInformation

In patients with acute myocardial infarction and ventricular paced rhythm, we found a more severe degree of underlying coronary artery disease in those who presented with a discordant ST-segment elevation greater than or equal to5 min on the admission electrocardiogram. There was no association between the electrocardiographic criterion and the angiographic findings on the culprit vessel; therefore, to better identify the patients who benefit from emergency reperfusion, we may need to exercise a low threshold to undertake coronary angiography in this population.

EchocardiographyVolume 19, Issue 1 p. 77-78 Paradoxical Embolism Nattawut Wongpraparut M.D., Nattawut Wongpraparut M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorManila Zaman M.D., Manila Zaman M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorNicholas Langan M.D., Nicholas Langan M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs M.D., Larry E. Jacobs M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler M.D., Morris N. Kotler M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorAlyson N. Owen M.D., Alyson N. Owen M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this author Nattawut Wongpraparut M.D., Nattawut Wongpraparut M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorManila Zaman M.D., Manila Zaman M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorNicholas Langan M.D., Nicholas Langan M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorLarry E. Jacobs M.D., Larry E. Jacobs M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorMorris N. Kotler M.D., Morris N. Kotler M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this authorAlyson N. Owen M.D., Alyson N. Owen M.D. Echocardiography Laboratory, Division of Cardiology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PennsylvaniaSearch for more papers by this author First published: 24 July 2003 https://doi.org/10.1046/j.1540-8175.2002.00077.xCitations: 2 Address for correspondence and reprint requests: Morris N. Kotler, M.D., Albert Einstein Medical Center, 363 Klein Professional Building, 5401 Old York Road, Philadelphia, PA 19141. Fax: 215 456-6189. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume19, Issue1January 2002Pages 77-78 RelatedInformation

Rapid progression of aortic stenosis was associated with 3 variables: patients on hemodialysis, those taking a calcium supplement, and those with elevated serum creatinine. Compared to patients with slow progression of aortic stenosis, rapid progressors should be followed closely with serial clinical and echocardiographic examinations.

We report the case of a 60-year-old woman with a history of ataxia who sought evaluation after a syncopal episode. A diagnostic workup revealed pulmonary emboli, pernicious anemia. (PA), hyperhomocysteinemia, and a G20210A prothrombin gene mutation. She was successfully treated with homocysteine-lowering therapy, including high doses of oral cobalamin. She also received oral anticoagulation for 6 months. At 1 year of follow-up, no further thrombotic episodes had occurred. Our report highlights the thrombotic risk of hyperhomocysteinemia secondary to PA in a patient with the G20210A prothrombin gene mutation.

BACKGROUND:Survival in patients with infective endocarditis (IE) ranges from 4 to 50% depending on the type of organism, the type of valve involvement and the type of treatment. METHODS:We conducted a retrospective analysis of data in hemodialysis (HD) patients at our center from 1990 to 2000. Demographics, risk factors, and outcome data were extracted in the subgroup of patients with first-episode IE diagnosed primarily by echocardiography. RESULTS:A total of 2239 patients underwent HD at our center. Thirty-two (1.4%) had IE defined using the Duke Criteria. Permanent and temporary venous dialysis catheters, arteriovenous (AV) grafts, and AV fistulae were used in 19 (59%), 12 (38%), and 1 (3%) patient respectively. Mean access duration was 7.6 +/- 7.9 months. Thirty (94%) patients had positive blood cultures, with the majority having Staphylococcus aureus bacteremia. Two (7%) patients had positive echocardiographic findings but negative blood cultures due to the commencement of empiric antibiotic therapy prior to blood cultures. The mitral valve was mainly affected. Transesophageal echocardiography was performed in 23 (72%) patients and detected an intracardiac mass in all 23 patients. One-year mortality was 56.3%. A poor 1-year prognosis was associated with presenting features of low hemoglobin, elevated leukocyte count, hypoalbuminemia, severe aortic and mitral regurgitation, and annular calcification in mitral valve IE. CONCLUSION:The prevalence of IE in HD patients is 1.4%. One-year mortality was 56.3%. Close observation is required during the first year when patients with severe valvular regurgitation and hematological abnormalities have a high mortality.

OBJECTIVE:Many prognostic variables have been studied in patients with Pneumocystis carinii pneumonia and acquired immunodeficiency syndrome (AIDS). The role of the electrocardiogram in this setting has not been previously evaluated. We analyzed the admission electrocardiogram in patients with Pneumocystis carinii pneumonia and AIDS in an attempt to identify electrocardiogram findings that could be associated with adverse clinical outcomes and worse prognostic variables. DESIGN:A retrospective medical chart review. SETTING:All confirmed cases of Pneumocystis carinii pneumonia in patients positive for human immunodeficiency virus admitted to Albert Einstein Medical Center from 1994 to 2000. METHODS:Patients were assigned increasing severity ranks based on the findings on the admission electrocardiogram (normal sinus rhythm, sinus tachycardia, and right ventricular strain pattern). Data were extracted regarding study outcomes (admission to intensive care unit, mechanical ventilation, and hospital mortality) and prognostic variables. MAIN RESULTS:Of the 40 study patients, 14 (35%) had normal sinus rhythm, 15 (37.5%) had sinus tachycardia, and 11 (27.5%) presented with signs of right ventricular strain. The number of admissions to the intensive care unit, use of mechanical ventilation, and hospital mortality rate all increased with the severity of the electrocardiogram findings (p < or =.03). The serum lactate dehydrogenase concentrations and the alveolar-arterial oxygen gradient both increased with the severity of the electrocardiogram findings (p < or =.02). CONCLUSION:Electrocardiogram findings of sinus tachycardia and right heart strain are common in Pneumocystis carinii pneumonia. These findings are associated with adverse clinical outcomes as well as worsening of prognostic variables. The electrocardiogram may be useful in predicting outcome in patients with Pneumocystis carinii pneumonia.