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Biomedical subjects

A Chauhan

Publications and source records attributed to A Chauhan.

At least 91 records · Page 5Linked to original sources
PubMed1995

Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty.

Early restenosis in over 30% of cases limits the benefits of percutaneous transluminal coronary angioplasty (PTCA). The mechanisms that underlie restenosis are uncertain, although experimental evidence suggests that the renin-angiotensin system is involved in the vascular response to angioplasty. An insertion(I)/deletion(D) polymorphism in the angiotensin-converting enzyme (ACE) gene, which influences plasma ACE level, has been associated with an increased risk of myocardial infarction in those with the DD genotype. To investigate whether this polymorphism influences the risk of restenosis after PTCA, 233 patients who underwent single-vessel angioplasty in the Subcutaneous Heparin and Angioplasty Restenosis Prevention (SHARP) study were genotyped for the I/D polymorphism and pre-PTCA, post-PTCA, and 4-month clinical and quantitative angiographic data were compared in the three genotype groups. The groups, (II 53, ID 117, and DD 63) were well matched for baseline clinical and both pre- and post-PTCA angiographic features. At 4-month follow-up there was no significant difference between the genotype groups with respect to any of the quantitative angiographic criteria of restenosis: minimal luminal diameter at the site of the angioplasty (DD 1.35 [SE 0.10] mm, ID/II 1.43 [0.05] mm, difference -0.08 [95% CI -0.30 to 0.14]), numbers of subjects with more than 50% diameter stenosis (DD 49%, ID/II 46%, relative risk 1.06 [0.79 to 1.43]), or the number of subjects with more than 50% loss of the acute diameter gain after PTCA (DD 54%, ID/II 43%, 1.26 [0.94 to 1.67]). Likewise, there was no difference in the number of subjects with angina or a positive exercise stress test. We conclude that, in patients undergoing elective PTCA, the I/D polymorphism in the ACE gene does not influence the extent of restenosis, and typing for the polymorphism will not be a useful predictor of risk before the procedure.

Adult↗
PubMed1995

Differential effects of spermine on phosphatidylinositol 3-kinase and phosphatidylinositol phosphate 5-kinase.

The metabolism of phosphoinositides plays an important role in the signal transduction pathways. We report here that naturally occurring polyamines affect the activities of phosphatidylinositol (PI) 3-kinase and PI 4-phosphate (PIP) 5-kinase differently. While polyamines inhibited the PI 3-kinase activity, they stimulated the activity of PIP 5-kinase in the order of spermine > spermidine > putrescine. Spermine inhibited the PI 3-kinase activity in a concentration-dependent manner with an IC50 of 100 microM. On the other hand, spermine (5 mM) stimulated the activity of PIP 5-kinase 2-3 fold. Kinetic studies of spermine-mediated inhibition of PI 3-kinase revealed that it was noncompetitive with respect to ATP. The effect of Mg2+ and PIP2 concentration on kinase activity was sigmoidal, with spermine inhibiting PI 3-kinase activity at all PIP2 concentrations. While 1 mM calcium stimulated PI 3-kinase activity at submaximal concentrations of Mg2+ (1.25 mM), inhibition was observed at optimal concentration of Mg2+ (2 mM). We propose that spermine may modulate the cellular signal by virtue of its differential effects on phosphoinositide kinases.

Adenosine Triphosphate↗
PubMed1995

The Subcutaneous Heparin and Angioplasty Restenosis Prevention (SHARP) trial. Results of a multicenter randomized trial investigating the effects of high dose unfractionated heparin on angiographic restenosis and clinical outcome.

OBJECTIVES: We sought to determine whether 12,500 IU of unfractionated heparin given subcutaneously twice daily for 4 months after percutaneous transluminal coronary angioplasty beneficially influences the subsequent rate of angiographic restenosis and the incidence of clinical events. BACKGROUND: Heparin has been shown to exhibit powerful antiproliferative effects against smooth muscle cells in several animal models. METHODS: A randomized trial with blinded data analysis was undertaken to assess the effect of unfractionated subcutaneous heparin on angiographic restenosis after coronary angioplasty. After successful angioplasty, patients were randomized to receive no heparin or 12,500 IU of heparin given subcutaneously twice daily for 4 months. Quantitative coronary angiography was performed before angioplasty, immediately after angioplasty and at follow-up ("early" [before 4 months] or electively [at 4 months]). RESULTS: The study group comprised 339 patients, 167 randomly assigned to receive heparin, 172 to receive no heparin. Repeat cardiac catheterization was performed in 90% of randomized patients. At early and elective restudy (mean 4.2 months), the mean +/- SD difference in minimal lumen diameter between the postangioplasty and follow-up measurement was -0.55 +/- 0.58 mm for the no heparin group and -0.43 +/- 0.59 mm for the heparin group (p = NS). Clinical events during the follow-up period did not differ significantly between groups: fatal myocardial infarction (1 patient in each group), coronary bypass grafting (5 patients in each group), repeat angioplasty (12 in the no heparin, 6 in the heparin group), angina at 4-month assessment (33% in the no heparin, 32% in the heparin group). CONCLUSIONS: Long-term treatment with high dose subcutaneous heparin (12,500 IU twice daily) for 4 months did not favorably influence angiographic or clinical outcome after coronary angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1995

The serum concentration of active transforming growth factor-beta is severely depressed in advanced atherosclerosis.

Recent evidence has led us to propose that transforming growth factor-beta (TGF-beta) is a key inhibitor of atherosclerosis. We show here that a population of patients with advanced atherosclerosis all have less active TGF-beta in their sera than patients with normal coronary arteries, with a fivefold difference in average concentration between the two groups. This correlation with atherosclerosis is much stronger than for other known major risk factors and it may therefore have important diagnostic and prognostic significance. Aspirin medication correlates with an increase in active TGF-beta concentration, indicating that therapeutic interventions for TGF-beta are possible.

Aged↗
PubMed1995

Syndrome X--angina and normal coronary angiography.

It is clear that angina pectoris with normal coronary arteries is a heterogeneous and ill-defined syndrome that encompasses different pathogenic entities. Differences in patient selection and in definition of 'syndrome X' has made comparison between different study groups rather difficult. Two decades of investigations have not revealed a specific cause of this syndrome. There is now a general belief that syndrome X probably encompasses several pathophysiological disease entities and the mechanisms involved in syndrome X remain to be fully elucidated.

Chest Pain↗
PubMed1994

Acute myocardial infarction in angiographically normal coronary arteries following induction of general anesthesia.

Coronary spasm may occur with angiographically normal and diseased coronary arteries. General anesthesia has been described only rarely as a triggering event for coronary artery spasm, and only once before in the presence of angiographically normal coronary arteries. We have now seen three patients presenting with acute ST-segment elevation following induction of general anesthesia with enzyme evidence of myocardial necrosis in two patients. Cardiac catheterization was performed in all three patients with one of the procedures performed on an emergency basis owing to hemodynamic compromise. All three patients demonstrated angiographically normal coronary arteries. The electrocardiograms and coronary arteriograms are presented, and possible mechanisms for the injury pattern seen on the electrocardiogram are discussed. Coronary vasospasm causing an acute injury pattern on the electrocardiogram can be caused by general anesthesia and has to be recognized promptly and treated appropriately to prevent more serious complications.

Anesthesia, General↗
PubMed1994

Atypical strain of hepatitis E virus (HEV) from north India.

Hepatitis E virus (HEV) infection was detected during an epidemic in North India. Virus particles present in the stool of an acutely ill patient (YAM-67) was transmitted intravenously into rhesus monkeys (M. mulata) and orally to a human volunteer. Virus-like particles (VLPs) of 32-34 nm were detected in the bile of monkeys and in the stools of the human volunteer by means of solid phase immune electron microscopy (SPIEM) with acute homologous and heterologous sera. The VLPs were confirmed to be HEV by a reverse transcription polymerase chain reaction (RT-PCR). Virus-like particles from human volunteer stools were passaged further into rhesus monkeys. A bimodal rise in aminotransferase levels were observed in the animals, and liver histopathology indicated mild to severe form of hepatitis. Further, SPIEM and RT-PCR analysis in monkey bile revealed presence of virus from 15 to 45 days post-inoculation. Rechallenge of the animals 6 months after recovery with the same viral inoculum failed to produce abnormal liver function tests indicating the presence of protective immunity during this period. The VLPs in the stool from the patient (YAM-67) with epidemic hepatitis were found to retain infectivity even after several cycles of freeze-thawing and exposure at 37 degrees C for 2 days. Moreover, these VLPs from the patient, human volunteer, and monkeys did not react with an anti-HEV chimpanzee serum from NIH, Bethesda, MD. These findings indicate that this North India isolate of HEV is an atypical strain of HEV. The present study further validates that the rhesus monkey is a suitable experimental model for HEV.

Animals↗
PubMed1994

Abnormal cardiac pain perception in syndrome X.

OBJECTIVES: The purpose of this study was to determine whether a diminished cardiac pain threshold contributes to chest pain in patients with syndrome X. BACKGROUND: There have been some reports of an altered pain perception in syndrome X. METHODS: Intracardiac catheter manipulation was performed in four groups of patients (syndrome X [group 1, 36 patients]; mitral valve disease and normal coronary arteries [group 2, 36 patients]; mitral valve disease and coronary artery disease [group 3, 36 patients]; and heart transplant recipients with normal coronary arteries [group 4, 36 patients]). Coronary flow velocity was measured in patients with syndrome X and in transplant recipients by use of an intracoronary Doppler catheter positioned in the left anterior descending coronary artery at intracardiac catheter manipulation. Coronary flow reserve in response to papaverine was also measured in patients with syndrome X and in transplant recipients. RESULTS: Intracardiac stimulation produced typical anginal chest pain in 34 group 1 (syndrome X) patients (94%). However, chest pain was produced only in five patients (14%) in group 2, seven patients (19%) in group 3 and no patients in group 4. There were no significant changes in coronary blood flow velocity associated with chest pain in group 1 patients. Coronary flow reserve in response to a hyperemic dose of intracoronary papaverine was significantly lower in the syndrome X group. There was no significant difference in the prevalence with which the stimulation tests produced chest pain in patients with syndrome X with an impaired coronary flow reserve or a positive radionuclide scan. CONCLUSIONS: The results of our study suggest that abnormal cardiac pain perception is a fundamental abnormality in syndrome X.

Adult↗
PubMed1994

Hyperinsulinemia, coronary artery disease and syndrome X.

OBJECTIVES: This study was conducted to compare the insulin responses to an oral glucose load in healthy volunteers and patients with syndrome X and patients with coronary artery disease. BACKGROUND: An abnormal coronary flow reserve has been reported in syndrome X by several investigators. However, its cause is not known. Recently, it has been suggested that elevated insulin levels in syndrome X may contribute to microvascular dysfunction. METHODS: Insulin responses to an oral glucose load (75 g) were compared in 17 patients with coronary artery disease, 17 patients with chest pain, positive exercise test findings, normal coronary arteries and impaired coronary flow reserve (syndrome X) and 17 healthy volunteers (control subjects). All were matched for age, gender and body weight. Patients with overt diabetes mellitus or hypertension were excluded. Venous blood samples were taken during fasting and at 30, 60, 90 and 120 min after the glucose load. Samples were analyzed for glucose, immunoreactive insulin and C peptides. RESULTS: There was no significant difference in the glucose levels at all sampling points among the three groups. The C peptide and immunoreactive insulin levels were significantly higher than values in the control group at 60, 90 and 120 min in the groups with syndrome X and coronary artery disease. The peak responses and the areas under the curve were also significantly greater in the latter two groups. There was no significant difference at all sampling points between the group with syndrome X and the group with coronary artery disease. CONCLUSION: Patients with syndrome X have stimulated hyperinsulinemia, which may contribute to the pathophysiology of syndrome X.

Blood Flow Velocity↗
PubMed1994

Interaction of protein kinase C and phosphoinositides: regulation by polyamines.

Phosphatidylinositol 4,5-bisphosphate (PIP2) activates protein kinase C (PKC) in the presence of phosphatidylserine and calcium. Recently it has been demonstrated that direct interaction of PKC with PIP2 in the absence of divalent cation inactivates this kinase. In the present study, the interaction of natural aliphatic polyamines with phosphoinositides was investigated for its possible relevance to PKC-mediated protein phosphorylation. PKC/phosphoinositide interaction was studied by monitoring the changes in (a) intrinsic fluorescence of the enzyme, and (b) PKC activity (protamine sulphate or histone III-S as substrate). All the phosphoinositides: PIP2, phosphatidylinositol 4-phosphate (PIP) and phosphatidylinositol (PI) inactivated PKC with an IC50 of 0.4 microM for PIP2, 5 microM for PIP and 10 microM for PI. Hydrogenated PIP2 behaved similarly to that of natural PIP2. Time-dependent studies showed very rapid inactivation of PKC by PIP2. The polyamines spermine and spermidine at physiological concentrations protected PKC from phosphoinositides-mediated inactivation when added prior to PKC interaction with phosphoinositides. Putrescine was least effective. Addition of spermine or spermidine to PKC/phosphoinositides incubation mixture did not reverse PKC activity indicating that the inactivation of PKC by phosphoinositides is irreversible. Fluorescence quenching experiments showed that phosphoinositides inactivate PKC by inducing conformational changes of the enzyme that are prevented by spermine. We propose that polyamines protect PKC and possibly other protein kinase from phosphoinositides-mediated inactivation, and that inactivation of protein kinases by phosphoinositides may not have physiological relevance.

Animals↗
PubMed1994

Early complications after dual chamber versus single chamber pacemaker implantation.

This study was performed to compare the frequency of early complications after single chamber versus dual chamber permanent pacemaker implantation. Early complication was defined as one occurring in the 6-week period following implantation. We prospectively analyzed consecutive pacemaker implantation from January 1987 to June 1993 at our regional center. All complications were also analyzed for the relationship to operator experience, the venous access route, and the presence of temporary pacing wire at the time of implantation of the permanent pacing system. A total of 2019 new pacemaker units were implanted during this period. 1733 patients (85.8%) received a VVI pacemaker and 286 (14.2%) a DDD unit. Wound infection occurred in 11 (0.6%) VVI patients and 6 (2.1%) DDD patients. Lead displacement occurred in 18 (1%) VVI patients and 15 (5.2%) DDD patients (11 [3.8%] atrial and 4 [1.4%] ventricular). There were 10 (0.6%) pneumothoraces, 9 (0.5%) hematomas requiring drainage, 1 (0.06%) chylocele, and 2 (0.1%) deaths in the VVI group. There were 2 (0.7%) pneumothoraces, 2 (0.7%) hematomas, and no deaths in the DDD group. There was no significant increase in complications for experienced infrequent implanters (< 12 systems per year). In both groups the subclavian approach was associated with a risk of pneumothorax when compared to the cephalic approach. The rate of wound infection was higher in patients who had a temporary pacing wire in place. The use of prophylactic antibiotics does not appear to affect the incidence of wound infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗
PubMed1994

Effect of transcutaneous electrical nerve stimulation on coronary blood flow.

BACKGROUND: Although neurostimulation has been shown to be of benefit in angina pectoris, the exact mechanism of its action is not clear. This study was performed to examine the effect of transcutaneous electrical nerve stimulation on coronary blood flow. METHODS AND RESULTS: The effect of transcutaneous electrical nerve stimulation was studied in 34 syndrome X patients (group 1), 15 coronary artery disease patients (group 2), and 16 heart transplant patients (group 3). Coronary blood flow velocity (CBFV) in the left coronary system was measured at rest and after a 5-minute stimulation period with a Judkins Doppler. There was a significant increase in the resting CBFV in group 1 (from 6.8 +/- 4.1 to 10.5 +/- 5.7 cm/s, P < .001) and group 2 (from 6.8 +/- 4.1 to 10.5 +/- 5.7 cm/s, P < .001). However, there was no significant change in the resting CBFV in group 3. There were no significant changes in the coronary arterial diameters as a result of neurostimulation. There was a significant decrease in the epinephrine levels in group 1 (from 79.6 +/- 17.8 to 58.5 +/- 17.5 ng/L, P = .01) and group 2 (from 102.2 +/- 27.2 to 64.1 +/- 19.1 ng/L, P = .01). CONCLUSIONS: Transcutaneous electrical nerve stimulation can increase resting coronary blood flow velocity. The findings suggest that the site of action is at the microcirculatory level and that the effects may be mediated by neural mechanisms.

Aged↗
PubMed1994

Is coronary flow reserve in response to papaverine really normal in syndrome X?

BACKGROUND: An impaired coronary flow reserve in syndrome X has been demonstrated by many studies. Recently, however, a normal coronary flow reserve in response to papaverine was reported, but the number of patients in these studies was small. The aim of this study was to investigate whether coronary flow reserve in response to intracoronary papaverine is really impaired in syndrome X. METHODS AND RESULTS: We investigated 53 syndrome X patients (typical angina, a positive exercise test, and completely normal coronary arteries on angiography) and 26 heart transplant patients with normal coronary arteries (control group). All antianginal medications were stopped 48 hours before the study. A 3.6F intracoronary Doppler catheter was positioned in the proximal left anterior descending coronary artery and was connected to a Millar velocimeter. The coronary blood flow velocity at rest and in response to a hyperemic dose of papaverine was measured. Coronary flow reserve was defined as the ratio of hyperemic coronary blood flow velocity in response to papaverine and resting coronary blood flow velocity. The coronary flow reserve (mean +/- SD) in the syndrome X group was 2.72 +/- 1.39. The coronary flow reserve in the control group was significantly higher at 5.22 +/- 1.26 (P < .01). In both groups there was no significant difference in the heart rate or the mean arterial pressure during the study. CONCLUSIONS: Our study shows that coronary flow reserve in response to intracoronary papaverine is impaired in syndrome X patients.

Adult↗
PubMed1994

Measurements of human coronary vascular impedance.

The aim of this study was to develop a method of measuring human coronary circulation impedance in a clinical setting. The authors measured coronary flow reserve (CFR) in 27 patients with chest pain and normal coronary arteries. A Judkins-style, 8F Doppler-tipped angiographic catheter was positioned in the left coronary ostium. Resting coronary flow velocity (RFV) and response to a hyperemic 12 mg intracoronary dose of papaverine (PFV) were measured. The signals were recorded by a recorder connected to a microprocessor with analogue-to-digital converter and a maths coprocessor. Using this the authors could obtain values for impedance at RFV (IR) and at PFV (IP). The CFR was defined as the ratio: PFV/RFV. An impedance index (II) was obtained as the ratio of coronary vascular impedance at peak hyperemia to the impedance at rest. The CFR was 3.2 +/- 1.2 and the II was 0.33 +/- 0.11. There was a strong inverse correlation between the CFR and the II (r = -0.9). The authors conclude that this new approach may allow a further insight into the coronary pathophysiology and may become useful in clinical cardiology, eg, in the assessment of heart transplant and Syndrome X patients.

Adult↗
PubMed1994

Hepatitis E virus: epidemiological, clinical and serological studies of north Indian epidemic.

BACKGROUND: A large waterborne epidemic of viral hepatitis occurred in the city of Karnal (Haryana) from February to April 1987. An attempt was made to study the epidemic clinically, serologically and etiologically. METHODS: A house-to-house search of the city was conducted for the detection of acute hepatitis cases. Patients willing to give blood samples for liver function tests were studied. RESULTS: A total of 1273 persons (0.79% of persons surveyed) were affected by viral hepatitis. Of the 477 clinically and biochemically documented cases, more than 75% were adults, while only 11% were less than 10 years old. Children below 15 years of age and females had a significantly higher incidence of anicteric hepatitis. Serological markers for acute hepatitis A and B viruses were absent in 85% of patients. Antibodies to hepatitis E virus (HEV) were detected in 84% of acute phase sera studied by indirect immunofluorescence assay. Liver biopsy showed characteristic features of cholangitic hepatitis. Three of 19 pregnant females who developed hepatitis died. No residual clinical or biochemical abnormality was detected in any of the patients followed up for 8 months. This epidemic correlated with the timing of unsupervised digging of lanes to provide new tap water connections to houses in the congested area of the city. This resulted in damage to the sewerage system and leakages which contaminated drinking water supply. CONCLUSION: HEV was transmitted by contaminated drinking water in this epidemic. Most affected individuals were adults, and recovered without sequelae. Affected pregnant women had a worse outcome.

Adolescent↗