Clinical developments in cardiac activation mapping.
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Analysis of the 12-lead electrocardiogram (ECG) provides important diagnostic and prognostic information in the long QT syndrome. The clinical diagnosis of long QT syndrome is determined by the presence of a QTc > or = 0.44 sec. A normal QTc does not exclude a family member from being a genetic carrier. The ECG patterns of depolarization, the ST segment and shape of the T-wave can provide important clues as to the affected gene, particularly in conjunction with clinical information as to the precipitating causes of syncope or cardiac events. In arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), the typical ECG pattern consists of T-wave inversion beyond lead V1. Evidence of right ventricular parietal block is manifest by a QRS duration in V1 > or = 110 msec and a longer QRS duration in the right then left precordial leads. Evidence of slow fractionated conduction is present as epsilon waves. The signal averaged ECG may show exceedingly long and low late potentials. Information regarding the risk of sudden death may also be obtained from the ECG. The ECG changes alone or in combination can provide strong evidence for the diagnosis of ARVC/D and helps to differentiate ARVC/D from right ventricular outflow tract (RVOT) tachycardia. The typical pattern of the ECG in the Brugada syndrome is ST segment elevation in the right precordial leads. This abnormality can be dormant and elicited by administration of drugs that cause Na channel blockade, such as ajmaline or type 1a or 1C antiarrhythmic drugs. Individuals who do not have the Brugada ECG findings at baseline but have this pattern induced by antiarrhythmic drugs are also at risk for sudden death. Further risk stratification may be obtained in the asymptomatic patients if ventricular fibrillation is induced at electrophysiological study.
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OBJECTIVE: The purpose of this study was to pilot test a self-administered chest pain questionnaire, a revised version of the Chest Discomfort Diary (CDD-R), in a sample of patients with chronic angina selected from a population known to have low literacy. DESIGN: The study design was descriptive and correlational. SAMPLE: The study used a convenience sample of 27 subjects with documented history of coronary artery disease and angina. Characteristics of the sample included a mean age of 56.3 years (SD, 12.4 years), 88.9% African-American, and 56.3% male, and 59.3% had a history of acute myocardial infarction. Approximately 28% had achieved a 9th-grade education or less, and reading levels ranged from 4th grade to 12th grade. Subjects completed the CDD-R, a 36-item instrument reflecting multiple dimensions of anginal chest pain. RESULTS: Descriptions of the location (left chest, 66.6%), character (pressure, 59.2%), and precipitants of chest pain (walking, 51.8%) were consistent with clinical descriptions of "typical angina." Other physical symptoms such as shortness of breath (88.8%) and fatigue (85.1%) were reported. Walking (55.5%) was the activity most frequently described as difficult to perform because of chest pain, with sublingual nitroglycerin (77.7%) the most frequently used and most effective chest pain relief strategy. CONCLUSION: The CDD-R adequately measured multiple characteristics of anginal chest pain. Further research is needed to establish construct validity of the CDD-R and to determine the feasibility of using the instrument to monitor changes over time in patients' chronic angina.
Microcultures containing single sympathetic principal neurons and small numbers of dissociated heart myocytes were prepared from newborn rats. After the transmitter properties of the neuron were studied by electrophysiological experiments, the microculture was examined with the electron microscope. Single neurons of either putative cholinergic or putative adrenergic character made morphological synapses on themselves (autapses), although only cholinargic autapses were detected electrophysiologically. Numerous axonal varicosities were present adjacent to the myocytes but no synaptic specializations were evident. After permanganate fixation to localize endogenous norepinephrine, the endings of neurons which appeared to secrete catecholamines contained many small granular vesicles, while the endings of neurons which appeared to secrete acetylcholine contained none. The endings of neurons which apparently secreted both catecholamines and acetylcholine contained only occasional small granular vesicles.
Prior studies using transient transfection assays in cultured avian and murine skeletal myotubes indicate that the proximal 2-kb segment of the 5' flanking region of the human myoglobin gene contains transcriptional control elements sufficient to direct muscle-specific and developmentally regulated expression of reporter genes. To examine the function of the human myoglobin gene promoter during development of skeletal and cardiac myocytes in the intact animal, a 2.0-kb myoglobin gene upstream fragment was fused to an Escherichia coli lacZ reporter gene and injected into fertilized mouse oocytes. beta-Galactosidase (beta-gal) activity was detected selectively in cardiac and skeletal myocytes of fetal and adult transgenic mice. A distinctive spatial pattern of myoglobin promoter activity was observed in fetal hearts: beta-gal staining was more pronounced within the left ventricular subendocardium than within the subepicardium and was essentially undetectable in the ventricular trabeculae or atria. Expression of endogenous myoglobin mRNA and protein, assessed by in situ hybridization and immunohistochemistry, demonstrated a similar spatial pattern. In contrast, hearts from adult transgenic mice demonstrated essentially homogeneous expression of beta-gal and of endogenous myoglobin mRNA and protein throughout the myocardium, including the trabeculae and atria. These data indicate that the 2.0-kb upstream region of the human myoglobin gene includes cis-acting regulatory elements sufficient to direct transgene expression during murine cardiac development that is myocyte-specific and responsive to positional cues in a similar manner to the endogenous myoglobin gene.
Clinical work in cardiac transplantation has focused on combating the major complications of this procedure, namely graft rejection and infection. Retrospective analyses suggest that prospective HLA typing, as is done in renal transplantation, may improve patient survival. Trials using FK 506 in cardiac transplantation have demonstrated some benefit using this agent over cyclosporine. Innovative immunologic interventions using novel monoclonal antibodies, methotrexate, total lymphoid irradiation, or photochemotherapy have shown promise in treating allograft rejection. Finally, prophylactic ganciclovir appears to prevent cytomegalovirus disease in seropositive transplant recipients; however, prevention of primary infection in seronegative patients may prove more difficult.
Cardiac transplantation has matured as a therapeutic intervention, allowing definitive treatment of critically ill children and adults with end-stage heart disease. The ongoing critical shortage of donor organs continues to deny hundreds of individuals access to this intervention. Accordingly, many of the most meaningful recent advances made in the field of cardiac transplantation involve means of expanding our donor pool. While current immunosuppressive regimens have been considerably successful in the management of acute cellular rejection, management of the problems of acute and chronic vascular rejection remains disappointing. Advances in this arena remain particularly urgent for physicians and surgeons involved in the care of heart transplant recipients.
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1. The efficacy of green tea extract (GTE) on serum and cardiac lipids was investigated in streptozotocin (STZ)-diabetic rats. 2. Diabetes was induced in rats by a single intraperitoneal injection of STZ (60 mg/kg bodyweight). Six weeks after the induction of diabetes, GTE was administered orally for 4 weeks (300 mg/kg bodyweight daily). Bodyweight, heart weight, heart weight : bodyweight ratio, blood glucose, serum and cardiac lipids were determined in experimental rats. 3. In diabetic rats, there was a significant decrease in bodyweight with an increase in heart weight : bodyweight ratio and blood glucose. Diabetic rats had significantly increased serum levels of cholesterol, triglycerides, free fatty acids and low-density lipoprotein-cholesterol (LDL-C) and decreased levels of high-density lipoprotein-cholesterol (HDL-C). In the hearts of diabetic rats, there was a significant increase in cholesterol, triglycerides and free fatty acids levels, with an increase in lipoprotein lipase activity. 4. The administration of GTE to diabetic rats resulted in significant recovery in bodyweight, heart weight : bodyweight ratio and blood glucose levels. The administration of GTE reduced cholesterol, triglyceride, free fatty acid and LDL-C levels, and increased HDL-C levels, in the serum of diabetic rats. In addition, GTE decreased cholesterol, triglyceride, free fatty acids levels and lipoprotein lipase activity in the myocardium of diabetic rats. These beneficial effects of GTE are ascribed to its antihyperglycaemic and hypolipidaemic activity. In conclusion, green tea can reduce the risk of cardiovascular disease in diabetes with a significant improvement in lipid metabolism.
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Recent advances in computed tomography have the potential to change the way imaging is performed in the detection of coronary artery disease. The current generation of scanners offers the ability to rapidly acquire thin sections in conjunction with the electrocardiogram, allowing for both anatomic and physiologic data to be obtained. These advancements hold the promise for a noninvasive means of directly evaluating the coronary arteries that can be applied in every day practice. This article reviews the advances in technology and their implications for imaging the heart.