A better control for ICD patients?
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Amiodarone↗
Biomedical subjects
B Bhambi
Publications and source records attributed to B Bhambi.
Accuracy and usefulness of atrial pacing in conjunction with transthoracic echocardiography in the detection of cardiac ischemia.
Transthoracic echocardiography combined with transesophageal atrial pacing was performed in a community outpatient setting and compared with single-photon emission computed tomography (SPECT) and with coronary arteriography to determine the accuracy and usefulness of the technique. Two groups were defined: group A consisted of 65 of 189 patients who underwent all 3 procedures within a 90-day period; group B consisted of 53 patients who had atrial pacing with transthoracic echocardiography. Seventy-one patients had previously undergone atrial pacing with simultaneous transesophageal echocardiography. Atrial pacing to induce abnormal wall motion as an indicator of ischemia was performed by increasing the double product to > 20,000. We obtained a sensitivity and specificity of 87% and 88% for group A and 72% and 80% for group B, respectively. We believe that transthoracic echocardiography with atrial pacing is indicated as a means of stress echocardiography in its own right, especially in nonambulatory and chronotropically incompetent patients, as well as in the presence of an ambiguous result on SPECT testing. It is highly accurate compared with our previous study with atrial pacing and simultaneous transesophageal echocardiography, better tolerated, more easily accepted, less invasive, and less costly. Thus, it is a useful stress modality in the detection of myocardial ischemia.
Adult↗
Identification of intracoronary thrombus and demonstration of thrombectomy by intravascular ultrasound imaging.
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Coronary Thrombosis↗
Cardiac fibroblasts are predisposed to convert into myocyte phenotype: specific effect of transforming growth factor beta.
Cardiac fibroblasts are mainly responsible for the synthesis of major extracellular matrix proteins in the heart, including fibrillar collagen types I and III and fibronectin. In this report we show that these cells, when stimulated by transforming growth factor beta 1 (TGF-beta 1), acquire certain myocyte-specific properties. Cultured cardiac fibroblasts from adult rabbit heart were treated with TGF-beta 1 (10-15 ng/ml) for different periods of time. Northern hybridization analysis of total RNA showed that cells treated with TGF-beta 1 for 24 hr expressed mRNA corresponding to sarcomeric actin mRNA. Immunofluorescence staining and light microscopy showed that cultured cardiac fibroblasts treated with TGF-beta 1 became stained with a monoclonal antibody to muscle-specific actin. After treatment of quiescent cells with TGF-beta 1, cell proliferation (as measured by [3H]thymidine incorporation) was moderately increased (1.5-fold, P less than 0.001). NIH 3T3 cells and human skin fibroblasts, treated with TGF-beta 1, did not express sarcomeric actin mRNA. Treatment of cardiac fibroblasts with the mitogenic agent phorbol 12-myristate 13-acetate or with norepinephrine, angiotensin II, or interleukin 1 beta did not induce myocyte-specific actin mRNA. Cultured cardiac fibroblasts at the subconfluent stage, when exposed to TGF-beta 1 in the presence of 10% fetal bovine serum, gave rise to a second generation of slowly growing cells that expressed muscle-specific actin filaments. Our findings demonstrate that cardiac fibroblasts can be made to differentiate into cells that display many characteristics of cardiac myocytes. TGF-beta 1 seems to be a specific inducer of such conversion.
Actin Cytoskeleton↗
Differential effects of transforming growth factor-beta 1 and phorbol myristate acetate on cardiac fibroblasts. Regulation of fibrillar collagen mRNAs and expression of early transcription factors.
Cardiac fibroblasts are responsible for synthesis and deposition of fibrillar collagen types I and III. Transforming growth factor-beta 1 (TGF-beta 1) has been proved to increase collagen biosynthesis in various systems, both in vivo and in vitro. We have investigated the effect of TGF-beta 1 on collagen gene expression in cultured cardiac fibroblasts and have compared this effect with that of a mitogenic agent, phorbol myristate acetate (PMA). The regulation of collagen types I and III gene expression was examined by using cDNA probes to rat alpha 2 (I) and mouse alpha 1 (III) procollagens. Quiescent cultured cardiac fibroblasts from rabbit heart were treated with TGF-beta 1 (10-15 ng/ml) and PMA (200 ng/ml). After 24 hours of treatment with TGF-beta 1, the abundance of mRNA for pro-alpha 2 (I) and pro-alpha 1 (III) collagens was increased by 112% (p less than 0.001) and 97% (p = 0.05), respectively, in treated fibroblasts compared with untreated cells. However, PMA-treated cells showed an opposite response: a 42% (p = 0.01) decrease in mRNA levels for pro-alpha 2 (I) collagen was observed. Immunofluorescent staining of cardiac fibroblasts in culture with anti-type I collagen antibody showed that alterations in mRNA levels led to altered collagen synthesis: cellular collagen was relatively increased in TGF-beta 1-treated cells and significantly diminished in PMA-treated cells. The abundance of mRNA for pro-alpha 1 (III) collagen was not affected by PMA treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of norepinephrine on myocardial collagen gene expression and response of cardiac fibroblasts after norepinephrine treatment.
Biosynthesis of the collagen matrix of the heart has been shown to be regulated under various physiologic and pathologic conditions. Biogenic amines have known effects on myocardial function. The authors studied the effects of norepinephrine on myocardial collagen gene expression in the rat heart. Norepinephrine was administered intravenously in a sustained-release manner. Within 1 hour after treatment, the abundance of mRNA for pro alpha 2 (I) collagen increased by 212% (P = 0.05), TGF-beta 1 by 91% (P = 0.05), and cytoskeletal actin by 429% (P less than 0.01) in the ventricular myocardium of the treated rats compared with that in control untreated rats. In extended period of treatment, the abundance of mRNA for pro alpha 2 (I) collagen reached a peak (206% increase, P less than 0.01) at day 3, remained elevated through day 6, and returned to the control levels at 2 weeks after treatment. The expression of mRNA for TGF-beta 1 was coregulated with that of pro alpha 2 (I) collagen. The abundance of mRNA for cytoskeletal actin showed a sharp increase (323%, P less than 0.05) at day 1 and remained elevated through day 6 in treated hearts compared with that in control hearts and returned to the control levels at 2 weeks after treatment. Coadministration of alpha-receptor blocker, phentolamine, led to modest reversal, whereas coadministration of beta-receptor blocker, propranolol, led to about 50% reversal of norepinephrine effects on the abundance of mRNAs. At day 3 of treatment, collagen content of ventricular tissue, as determined by hydroxyproline measurement was increased by 13% (P less than 0.05) in treated hearts. Immunofluorescent light microscopy showed increased collagen deposition and focal areas of necrosis in the endocardial regions in hearts of animals treated with norepinephrine for 2 weeks. In vitro studies on cultured cardiac fibroblasts showed that although norepinephrine treatment does not lead to significant changes in the abundance of mRNA for pro alpha 2 (I) collagen, it leads to increased mRNA for cytoskeletal actin and increased (113%, P less than 0.05) 3H-thymidine incorporation into the cell nuclei of treated cells compared with that in untreated cells. The authors conclude that although norepinephrine has no direct in vitro effects on collagen type I biosynthesis, its in vivo effects may lead to a cascade of events such as induction of growth factors that ultimately result in increased expression of collagen type I in the myocardium.
Actins↗