Home About us Contact
|
Home About us Contact | ||
|
|
||
Myocardial Disease (myocardial + disease)
Selected AbstractsRecurrent Ventricular Tachycardia in Patient with Friedreich's Ataxia in the Absence of Clinical Myocardial DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2010NIDAL ASAAD M.B.B.S. We report a 33-year-old man with recurrent loss of consciousness due to ventricular tachyarrhythmia with a history of Friedreich's ataxia. The patient's symptom was improved after implantation of a single-lead implantable cardiac defibrillator. The clinical, genetic, echocardiographic, and electrocardiographic features are discussed in brief. (PACE 2010; 33:109,112) [source] Left Ventricular Non Compaction in ChildrenCONGENITAL HEART DISEASE, Issue 5 2010Sara H. Weisz MD ABSTRACT Left ventricular non compaction (LVNC) is a myocardial disease characterized by a hypertrabeculated myocardium. The hypertrabeculations in the left ventricular wall define deep recesses communicating with the left ventricular chamber where blood penetrates with increased risk of blood clots in the meshwork of the prominent trabeculations. The left ventricular apex and the free wall are particularly affected. During in utero ventriculogenesis, myocardial blood supply is initially linked to the presence of sinusoids, in which blood penetrates and diffuses nutriments and oxygen to myocardial cells. Progressively, with the development of the heart and the increase of cells demand of blood, coronary arteries system develops. This step is associated with myocardial modification that leads to compaction of hypertrabeculated myocardial net. Probably, the premature interruption of this process leads to ventricular noncompaction. Many studies have been conducted in adults with hypertrabeculated myocardium. To date, data regarding childhood LVNC are sparse. The aim of this review is to summarize the clinical and preclinical knowledge about LVNC in children. [source] Cardiac amyloidosis in a patient with multiple myeloma: A case report and review of literatureJOURNAL OF CLINICAL ULTRASOUND, Issue 3 2009David Sedaghat MD Abstract We report a case of a 52-year-old man with multiple myeloma and rapidly progressive heart failure who died unexpectedly from a probable arrhythmia. Postmortem examination revealed infiltrative amyloid cardiomyopathy, a rare cause of predominantly diastolic myocardial disease. Cardiac amyloidosis should be considered in any patient presenting with congestive heart failure, preserved systolic function, and a discrepancy between a low QRS voltage on electrocardiography and an apparent left ventricular hypertrophy on sonogram. The pattern of left ventricular diastolic dysfunction changes during the course of amyloidosis and the classically described restrictive physiology occurs only in advanced stages of the disease. © 2009 Wiley Periodicals, Inc. J Clin Ultrasound, 2009 [source] Cardiac amyloidosis: MR imaging findings and T1 quantification, comparison with control subjectsJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 6 2007Gabriele A. Krombach MD Abstract In cardiac amyloidosis an interstitial deposition of amyloid fibrils causes concentric thickening of the atrial and ventricular walls. We describe the results of tissue characterization of the myocardium by T1 quantification and MRI findings in a patient with cardiac amyloidosis. The T1 time of the myocardium was elevated compared to that in individuals without amyloidosis. The T1 time of the myocardium was 1387 ± 63 msec (mean value obtained from four measurements ± standard deviation [SD]) in the patient with cardiac amyloidosis, while the reference value obtained from the myocardium of 10 individuals without known myocardial disease was 1083 ± 33 msec (mean value ± SD). In combination with other MR findings suggestive of amyloidosis, such as homogeneous thickening of the ventricular and atrial walls, thickening of the valve leaflets, restrictive filling pattern, and reduction of systolic function, T1 quantification may increase diagnostic confidence. J. Magn. Reson. Imaging 2007;25:1283,1287. © 2007 Wiley-Liss, Inc. [source] Spontaneous resolution of hypothermia-induced atrial fibrillation in a dogJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2004Scott A. Campbell DVM Abstract Objective: To report a case of spontaneous resolution of atrial fibrillation secondary to hypothermia in a dog without detectable heart disease. Case summary: An 8-year-old female spayed mixed breed dog presented with a history of prolonged exposure to below freezing environmental temperatures. The dog presented hypothermic (<32°C or <90°F) and minimally responsive to stimuli. The heart rate was 80 beats per minute (bpm) and irregular. Atrial fibrillation was diagnosed. The dog had pale mucous membranes, absent femoral pulses, and no obtainable blood pressure via indirect Doppler technique. Resuscitation fluids were administered and active external warming was instituted. Peripheral edema was observed during the rewarming phase and the irregular heart rate was noted to increase. The atrial fibrillation spontaneously resolved with no specific anti-arrhythmic therapy. No underlying myocardial disease was found. The recovery of this dog was complete with a subsequent repeat of the echocardiogram and electrocardiogram (ECG) 8-months later found to be within normal limits. [source] Loeffler endocarditis: What have we learned?AMERICAN JOURNAL OF HEMATOLOGY, Issue 10 2007Juan Benezet-Mazuecos Loeffler endocarditis, eosinophilic endomyocardial disease or fibroplastic endocarditis appears to be a subcategory of the Hypereosinophilic syndrome in which the heart is predominantly involved. It is an uncommon myocardial disease, thought to be secondary to eosinophils damage, characterized by fibrous thickening of the endocardium of one or both ventricles, leading to apical obliteration and multiple cardiovascular complications. Despite all the efforts, the ultimate responsible mechanisms of this entity remain unresolved. Many theories have been raised trying to explain this phenomenon, but nowadays the enigma in relation to the different patterns of evolution continues. In this concise review we discuss the different pathophysiologic theories postulated and the management of the cardiovascular complications. Perhaps it will serve to assist in recognition of patients with the same condition around the world. Am. J. Hematol. 82:861,862, 2007. © 2007 Wiley-Liss, Inc. [source] Asymptomatic myocardial ischemic disease in antiphospholipid syndrome: A controlled cardiac magnetic resonance imaging studyARTHRITIS & RHEUMATISM, Issue 7 2010Karim Sacré Objective Antiphospholipid syndrome (APS) may cause coronary thrombosis. This study was undertaken to determine the prevalence of silent myocardial disease in patients with APS, using late gadolinium enhancement (LGE) of cardiac magnetic resonance imaging (CMRI). Methods Twenty-seven consecutive patients with APS and 81 control subjects without known cardiovascular disease underwent CMRI. The prevalence of occult myocardial ischemic disease, as revealed by LGE, was compared between patients with APS and controls, and factors associated with myocardial disease were identified in patients with APS. Results Myocardial ischemic disease, as characterized by LGE on CMRI, was present in 8 (29.6%) of 27 patients with APS, and imaging with LGE showed a typical pattern of myocardial infarction (MI) in 3 patients (11.1%). The myocardial scarring revealed on CMRI was not detected by electrocardiography or echocardiography. Although both patients with APS and control subjects shared a low risk of cardiovascular events, as calculated with the Framingham risk equation (mean ± SD 5.1 ± 8.2% and 6.5 ± 7.6%, respectively, for the absolute risk within the next 10 years; P = 0.932), the prevalence of myocardial ischemia was more than 7 times higher in patients with APS (P = 0.0006 versus controls). No association was found between myocardial disease in patients with APS and classic coronary risk factors. The presence of myocardial scarring tended to be more closely associated with specific features of APS, such as duration of the disease, presence of livedo, and positivity for anti,,2 -glycoprotein I antibodies. Conclusion The finding of a significant and unexpectedly high prevalence of occult myocardial scarring in patients with APS indicates the usefulness of CMRI with LGE for the identification of silent myocardial disease in such patients. [source] | |||||||||||||||||||