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Biomedical subjects

A C Jain

Publications and source records attributed to A C Jain.

At least 19 recordsLinked to original sources
PubMed2001

Hygroscopicity, phase solubility and dissolution of various substituted sulfobutylether beta-cyclodextrins (SBE) and danazol-SBE inclusion complexes.

The aim of the present work was to characterize hygroscopicity, phase solubility and dissolution properties for various substituted sulfobutylether beta-cyclodextrins (SBEs) and danazol-SBE inclusion complexes. Moisture sorption was measured using a symmetric gravimetric analyzer. The complexes were characterized by powder X-ray diffraction (XRD) and differential scanning calorimetry (DSC). Moisture sorption isotherms for the SBEs and the complexes showed low moisture sorption at RH <60%. The moisture absorption desorption isotherms for the various SBEs showed very little hysteresis, indicating almost complete desorption. Moisture adsorbed by the various SBE was in the order SBE 7>SBE 4>SBE 5 at 95% RH. Powder XRD data for complexes showed the disappearance of characteristic crystalline peaks for danazol or the formation of amorphous entities and DSC showed the disappearance of the peak of fusion of danazol indicating complex formation. Phase solubility of danazol with various substituted SBEs indicated 1:1 stoichiometry of complexes. The apparent stability constant, as determined by the method of Higuchi and Connors, increased as the degree of substitution of SBEs increased and decreased as the temperature increased. The dissolution of the complexes was significantly greater than that of the corresponding physical mixtures indicating that the formation of amorphous complex increased the solubility of poorly soluble danazol. More than 85% of danazol was released in <10 min, compared to 15% danazol release from the physical mixtures.

Calorimetry, Differential Scanning↗
PubMed2000

Randomized comparison of elective stent implantation and coronary balloon angioplasty guided by online quantitative angiography and intracoronary Doppler. DESTINI Study Group (Doppler Endpoint STenting INternational Investigation).

BACKGROUND: The purpose of this study was to compare long-term outcomes of coronary stenting in all lesions (elective stenting) or only in lesions with inadequate morphological and functional results after balloon angioplasty (guided PTCA). METHODS AND RESULTS: Treatment of multivessel disease, with any lesion length and vessel size, was allowed provided that all lesions were suitable for stent implantation. Patients were randomized to elective stent implantation (n=370) or guided PTCA (n=365). An optimal PTCA result (residual diameter stenosis </=35%, coronary flow reserve measured with a Doppler guidewire >2.0, absence of threatening dissections) was achieved in 166 lesions (43%). The remaining 218 lesions underwent stent implantation (provisional stenting). Final residual diameter stenosis was lower in the elective and provisional stent groups (9.3% and 10.2%) than in the optimal PTCA group (24.8%, P:<0. 00001). On an intention-to-treat analysis, the probability of >/=1 major adverse cardiac event at 12 months was 17.8% in the elective stenting group and 18.9% in the guided PTCA group (20.1% for optimal PTCA and 18.0% for the provisional stenting subgroup, P:=NS). The incidence of repeat target lesion revascularization at 1 year was 14. 9% in the elective stent group and 15.6% in the guided PTCA group (17.6% for optimal PTCA and 14.1% for the provisional stenting subgroup, P:=NS). CONCLUSIONS: When balloon angioplasty is guided by online quantitative angiography and Doppler-derived coronary flow reserve, with provisional stenting reserved for suboptimal results, early and late clinical outcomes are comparable to those achieved by elective stenting of all patients.

Angiography↗
PubMed2000

Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block.

The objective of this study was to identify left atrial (LA) abnormality on the electrocardiogram and other related variables as predictors of left ventricular (LV) hypertrophy in the presence of left bundle branch block (LBBB). In the presence of complete LBBB, the diagnosis of electrocardiographic abnormalities is problematic and that of LV hypertrophy remains difficult. The usual electrocardiographic criteria applied for the diagnosis of LV hypertrophy may not be reliable in the presence of LBBB. Therefore, noninvasive criteria will help physicians diagnose LV hypertrophy with electrocardiography. LA abnormality on the electrocardiogram was assessed by 2 independent observers as predictor of LV hypertrophy in the presence of LBBB in 120 patients, and data were compared with those of 100 patients without LA abnormality. LV mass was calculated from echocardiographic data. Besides LA abnormality, the other variables studied for prediction of LV hypertrophy were gender, age, body surface area, body mass index, frontal axis, and QrS duration. Of the 6 criteria analyzed, the P terminal force was found to be the most common and consistent criterion to detect LA abnormality. LV hypertrophy was confirmed by echocardiographic determination of LV mass in both groups. Observers reliably differentiated between the hypertrophied and normal-sized left ventricle in the presence of LBBB by correlating LA abnormality with LV mass determined by echocardiography. Observer 1 detected LA abnormality in 89% and observer 2 in 84% of patients. False-positive results were present in 11% and 16%. The observer's recognition of LA abnormality in the present study was 91%. The 2 observers showed a sensitivity of 81% and 79% and a specificity of 91% and 88%, respectively, when diagnosis of LV hypertrophy was determined. LV mass increased significantly and was diagnostic of LV hypertrophy in 92% of patients with LA abnormality. In the remaining 11 patients (8%), the LA abnormality was of marginal abnormal magnitude. Each 0.01-mV/s increase in LA abnormality gave an increase of 30 g of LV mass. LV mass was increased in 86% of patients when corrected by body surface area. LV hypertrophy in the presence of LBBB on electrocardiography was found in only 13 patients (10%) when the 6 frequently used conventional criteria for diagnosis of LV hypertrophy by electrocardiography were used. Regression analysis revealed LA abnormality to be a strong independent predictor of increased LV mass. Multivariate analysis also revealed age, body mass index, body surface area, frontal axis, and QrS duration to be significant predictors of LV mass. This noninvasive study correlates LA abnormality by electrocardiogram and LV hypertrophy with echocardiography to conclude that LA abnormality was significantly diagnostic of LV hypertrophy in the presence of LBBB. Age, body mass index, body surface area, frontal axis, and QrS duration were also significant predictors of LV mass.

Adolescent↗
PubMed1999

Early repolarization.

Early repolarization (ER) is an enigma. The purpose of this review is to reemphasize the overall electrocardiographic (ECG) pattern of this normal ST variant which continues to challenge the clinician because of its similarity to the current of injury potential to myocardium or an acute pericarditis. The data were provided from the studies identified through computerized searches of Medline, Toxline, Oxford, Agricola, and Bios Afterdark, Cumulative index, and a review of bibliographies of relevant articles on the related subjects. Early repolarization has elevated, upward, concave ST segments, located commonly in precordial leads, with reciprocal depression in a VR, tall, peaked and slightly asymmetrical T waves with notch, and slur on the R wave. The other accompanying features in the ECG are vertical axis, shorter and depressed P-R interval, abrupt transition, counterclockwise rotation, presence of U waves, and sinus bradycardia. Males dominate and patients are often younger than 50 years of age. The incidence of 1 to 2% is found equally common in all races. Degree and incidence of ST elevation decrease as age advances. Exercise or isoproterenol administration may normalize the ST segment. Early repolarization is a benign condition. If the ECG conforms to a classical pattern of ER on serial ECGs, it would exclude the unnecessary hazards of present day revascularization therapy for myocardial infarction such as primary angioplasty or thrombolytic therapy, or aggressive management of acute pericarditis, and so forth. This review concludes with a discussion of comparative ECG features of ER, pericarditis, and myocardial infarction, and provides an algorithm for diagnostic management of patients suffering from these conditions.

Acute Disease↗
PubMed1999

Constrictive pericarditis.

The diagnosis of constrictive pericarditis remains a challenge because its physical findings and hemodynamics mimic restrictive cardiomyopathy. Various diagnostic advances over the years enable us to differentiate between these two conditions. This review begins with a case report of constrictive pericarditis, followed by a brief history and discussions of etiologies. Clinical features, radiologic, electrocardiographic, angiographic findings, and hemodynamics of constrictive pericarditis are reviewed. The echocardiographic findings are detailed and the recent advances in Doppler flow velocity patterns of pulmonary, mitral, tricuspid valves and hepatic veins are reported. Nuclear ventriculograms depict rapid ventricular filling in constrictive pericarditis and differentiate it from restrictive cardiomyopathy. Endomyocardial biopsy helps further in recognizing the various types of restrictive cardiomyopathies. Computed tomography and magnetic resonance imaging delineate abnormal pericardial thickness in constrictive pericarditis. Association of characteristic hemodynamic changes and abnormal pericardial thickness > 3 mm usually confirms the diagnosis of constrictive pericarditis. Effusive and occult varieties of constrictive pericarditis are briefly described. This review concludes with emphasizing the importance of pericardial resection.

Adult↗
PubMed1999

Combined effects of caffeine and alcohol on hemodynamics and coronary artery blood flow in dogs.

Alcohol intake is often followed by coffee drinking because of the universal acceptance of its sobering effect. Such effects were found inconsistent on motor functions. However, it is common belief that caffeine will antagonize the intoxicating effects of alcohol. The independent actions of caffeine and alcohol are well documented, but combined effects of short-term administration are unknown. This experimental work was designed to study the effects due to short-term administration of caffeine and alcohol on the cardiovascular system. In phase I, 30 experiments were performed in our laboratories to study the dose-response curves of both the drugs. In phases II and III, 15 dogs were subjected to 30 experiments. In phase II, caffeine, 5 mg/kg, was given i.v., followed by ethanol, 400 mg/kg i.v., and in phase III, sequence of drug administration was reversed to study the effects on hemodynamics and coronary artery blood flow. Caffeine did not show significant changes in all the cardiovascular parameters, and ethanol administration caused nonsignificant increase in heart rate, mean arterial pressure, left ventricular systolic pressure, and left ventricular (LV) mechanical work and decrease in the maximal rate of first derivative of LV pressure, stroke volume, and systemic vascular resistance. Left ventricular end-diastolic, pulmonary artery mean and right atrial pressures, pulmonary vascular resistance, myocardial oxygen consumption, and as coronary flow reserve increased as compared with controls. Combined caffeine and alcohol had synergistic effects, but when the order of drug administration was reversed (i.e., alcohol was followed by caffeine), the effect was antagonistic.

Animals↗
PubMed1998

Left atrial abnormality by electrocardiogram predicts left ventricular hypertrophy by echocardiography in the presence of right bundle-branch block.

BACKGROUND: Left ventricular hypertrophy (LVH) on the electrocardiogram (ECG) may be masked in the presence of complete right bundle-branch block (RBBB). Left bundle-branch block on the ECG is associated with LVH at autopsy in 93% of hearts studied. However, RBBB does not predict LVH and the usual ECG criteria applied for LVH may not be reliable in the presence of RBBB. HYPOTHESIS: The study was undertaken to evaluate left atrial (LA) abnormality as a criterion for the diagnosis of LVH in the presence of RBBB. METHODS: Left atrial abnormality in the ECG was assessed by two independent observers as a criterion of LVH in the presence of RBBB in 100 patients, and data were compared with those of 50 patients without LA abnormality. RESULTS: Left ventricular hypertrophy was confirmed by echocardiographic determination of left ventricular (LV) mass in both groups. Observers reliably differentiated between hypertrophied and normal-sized LV in the presence of RBBB by using LA abnormality as an ECG criterion when correlated with LV mass determined by echocardiography. Observer 1 correctly detected LVH in 88% and Observer 2 in 82% of patients. False positive diagnosis was made in 12 and 18% of patients by Observers 1 and 2, respectively. Observers' performance of recognition of LA abnormality in the present study was 94%. Results showed sensitivity of 76 and 70% and specificity of 84 and 92% for Observers 1 and 2, respectively. Left ventricular mass increased significantly and was diagnostic of LVH in 92% of patients with LA abnormality. Left ventricular mass was high in 84% of patients when corrected by body surface area. LVH in the presence of RBBB by the ECG was found in only seven patients (5%) when six commonly used conventional criteria of diagnosis of LVH by ECG were employed. Regression analysis found LA abnormality to be a strong independent predictor of increased LV mass. Multiple regression analysis revealed that age, body mass index, body surface area, and frontal axis are also significant predictors of LV mass. CONCLUSION: The results obtained by the correlation of LA abnormality by ECG and LVH by echocardiography conclude that LA abnormality by ECG was significantly diagnostic of LV hypertrophy in the presence of RBBB.

Adolescent↗
PubMed1998

Combined effects of alcohol and nicotine on cardiovascular performance in a canine model.

Alcohol and tobacco consumption are correlated. Smokers consume more alcohol than do nonsmokers, and alcohol consumers smoke more than do teetotalers. The independent effects of alcohol and nicotine on the cardiovascular system are well documented, but combined effects of short-term administration are unknown. This experimental work was designed to study the effects due to short-term administration of alcohol and nicotine on cardiovascular system. In phase I, 30 experiments were performed to study the dose-response curve of both the drugs. In phases II and III, 15 dogs were subjected to 30 experiments. In phase II, ethanol, 400 mg/kg, was given i.v., followed by nicotine 50 microg/kg, i.v., and in phase III, sequence of drug administration was reversed to study the effects on hemodynamics and coronary artery blood flow. The dose-response curve established the i.v. dose of ethanol, 400 mg/kg, and nicotine, 50 microg/kg. Ethanol administration caused a nonsignificant increase in heart rate (HR), mean arterial pressure (MAP), left ventricular systolic pressure (LVS), and left ventricular mechanical work (LVMW), and a decrease in maximal rate of increase of LV pressure per second (dP/dt), stroke volume (SV), and systemic vascular resistance (SVR). Left ventricular end-diastolic pressure (LVEDP), pulmonary artery mean pressure (PAM), right atrial pressure (RAP), pulmonary vascular resistance (PVR), myocardial oxygen consumption (MVO2), and average peak velocity of coronary blood flow (APV) had mild significant increases as compared with controls. Nicotine significantly increased heart rate, mean arterial pressures, LVEDP, and pulmonary artery, pulmonary capillary wedge, and right atrial pressures. Nicotine increased dP/dt (2,062-3,188; p < 0.006) and decreased APV (9 to 8; p < 0.03). Combined ethanol followed by nicotine had synergistic increase in HR, SD, MAP, LVS, LVEDP, pulmonary pressures, CO, SV, dP/dt (2,184 > 5,206; p < 0.005), MVO2, and LVMW. However, the excitatory effects of nicotine were attenuated when ethanol was administered after nicotine (dP/dt, reduced from 2,058 to 1,653; p < 0.04, and APV increased from 10 to 12; p < 0.02). We conclude that ethanol increased APV but had nonsignificant effects on the hemodynamics, whereas nicotine reduced the APV and had significant excitatory responses. In combination (i.v.), ethanol + nicotine produced significant synergistic excitatory effects. On the other hand, the nicotine + ethanol combination increased APV and caused attenuation of the excitatory effects of nicotine in dogs.

Animals↗
PubMed1998

Characteristics of West Virginians having myocardial infarction.

BACKGROUND: Prevalence of risk factors in patients having myocardial infarction (MI) have been reported in large US and international studies, but little is known about the prevalence of risk factors in West Virginians having MI. METHODS: Risk factors for MI were identified by ICD-9 codes. Logistic regression analysis was used to compute odds ratios and 95% confidence intervals. RESULTS: In this cohort (n = 727), 72% of men less than 65 years old were current smokers. Women were older and had a lower frequency of smoking and a higher frequency of diabetes mellitus and obesity than men. Women less than 65 years old had significantly more hypertension than men. CONCLUSIONS: In West Virginia, women who have MI are more likely to be nonsmoking diabetics with hypertension.

Adult↗
PubMed1997

Left atrial abnormality in acute myocardial infarction.

This study assessed left atrial abnormality by electrocardiogram as a predictor of left ventricular dysfunction during acute myocardial infarction. Hemodynamic, angiocardiographic, echocardiographic, and serial creatine kinase-MB studies revealed the electrocardiogram to be a significant predictor of location of acute myocardial infarction, prevalence of occlusive disease in coronary vessels, myocardial contractility, low ejection fraction, increased left ventricular end-diastolic pressure, and serial creatine kinase-MB.

Adult↗
PubMed1997

Combined effects of caffeine and nicotine on cardiovascular hemodynamics in canine model.

The independent effects of caffeine and nicotine on cardiodynamics are well documented, but combined effects of both are not reported. Initially, in phase I, 18 experiments were performed to study the dose-response curve of both the drugs. In phases II and III, 13 mongrel dogs were subjected to 30 experiments. In phase II, caffeine, 5 mg/kg, was given i.v. followed by nicotine, 50 micrograms/kg, and in phase III, the sequence of drug administration was reversed to study the effects on hemodynamics. In phase II, caffeine did not show significant changes in all the cardiovascular parameters, but nicotine administration after caffeine produced marked significant synergistic excitatory effects: the rate of increase of the first derivative of left ventricular pressure (dP/dt) increased from 1,101 +/- 111 to 3,194 +/- 872 (p < 0.003). In phase III, nicotine significantly increased heart rate, mean arterial pressures; left ventricular end-diastolic pressure (LVEDP); and pulmonary artery, pulmonary capillary wedge, and right atrial pressures. Nicotine increased dP/dt (964 +/- 182 to 1,639 +/- 60 mm Hg/s; p < 0.004). The excitatory effects of nicotine were attenuated by administration of caffeine (dP/dt, 918 +/- 140 reduced to 715 +/- 144 mm Hg/s; p < 0.04). Caffeine and nicotine, alone, caused nonsignificant and significant increases in hemodynamics, respectively. In combination, caffeine + nicotine administration produced significant synergistic excitatory effects in dogs. On the other hand, the nicotine + caffeine combination caused attenuation by caffeine of the excitatory effects produced by nicotine.

Animals↗
PubMed1997

Caffeine and cardiac arrhythmias. An experimental study in dogs with review of literature.

In spite of widespread belief among clinicians that caffeinated drinks are linked with palpitations, tachycardia and dysrhythmia there is paucity of documentary evidence. We investigated the arrhythmogenic activity of caffeine in canine model. The alkaloid was given i.v. to perform 51 experiments in 13 anesthetized dogs in three different doses. The Low dose generated significant Sinus (S) bradycardia (70%; p < 0.006, S. arrhythmia (70%; p < 0.02), S. arrest (50%; p < 0.04), Atrial (A) ectopics (40%; p < 0.016), Wandering of pacemaker (WPM) (50%; p < 0.04), and Ventricular premature contractions (VPC--unifocal 40%; p < 0.05) as compared with control ECGs. Medium dose induced significant S. arrhythmia (62%; p < 0.001), A. ectopics (25%; p < 0.01), A. tachycardia (25%; p < 0.01), WPM (25%; p < 0.01), VPCs--unifocal (50%; p < 0.002), multifocal (25%; p < 0.01), couplets (25%; p < 0.01) and interpolated (25%; p < 0.01). High dose of caffeine revealed significant S. arrhythmia (56%; p < 0.002), A. ectopics (44%; p < 0.005), A. tachycardia (32%; p < 0.01), WPM (32%; p < 0.01) and VPCs--unifocal (64%; p < 0.001), multifocal (32%, p < 0.01), couplets (32%, p < 0.01), interpolated (32%; p < 0.01) and Ventricular tachycardia (VT) (20%; p < 0.01). A. flutter and fibrillation each were observed in two experiments only. In conclusion, these data indicate a dose dependent arrhythmogenecity of caffeine. Small dose, mostly, generated, benign arrhythmias due to vagal stimulation. More severe arrhythmias like VT, multifocal VPC. A. flutter and A. fibrillation were generated with higher dose of caffeine. Mechanism remains uncertain as caffeine has multiple actions. Further studies in human beings with normal and compromised myocardium may elucidate arrhythmogenic effects of caffeine.

Animals↗
PubMed1995

Early repolarization on scalar electrocardiogram.

Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1-5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in a VR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

Adolescent↗
PubMed1994

Differential diagnosis of wide QRS tachycardias.

This article has reviewed the differential diagnosis of wide QRS tachycardia. We have found the stepwise approach suggested by Brugada to be very useful. Of the newer criteria that he proposes, the R to S interval of > 100 ms. appears to be a particularly helpful clue favoring the diagnosis of ventricular tachycardia. Hemodynamic stability, young age, 1:1 AV association, and the absence of structural heart disease do not exclude a diagnosis of ventricular tachycardia. Most wide QRS tachycardias in adults are ventricular, and when all else fails, one will be right more often than not in favoring this as the diagnosis over supraventricular tachycardia with aberrancy. The R to S interval is measured in the precordial (V) leads from the onset of the R wave to the deepest part of the S wave. A value > 100 ms. in any V lead strongly favors ventricular tachycardia. Example is from Case 1 (upper tracing is V1).

Diagnosis, Differential↗
PubMed1993

Myocardial infarct artery patency and reocclusion rates after treatment with duteplase at the dose used in the International Study of Infarct Survival-3. Burroughs Wellcome Study Group.

Duteplase, 98% double-chain recombinant tissue-type plasminogen activator, was administered intravenously in 488 patients with acute myocardial infarction in a multicenter, open, safety and patency study. Duteplase dosing was based on body weight. Duteplase was administered as a bolus of 0.04 MIU/kg of thrombolytic activity followed by 0.36 MIU/kg over 1 hour and 0.067 MIU/kg/hour for 3 additional hours. The patency rate of the infarct-related artery at 90 minutes was 69% (330 of 478). The reocclusion rate at 3 to 48 hours was 6% (18 of 301). Reinfarction occurred in 7.6% of patients (37 of 488), but 12 reinfarctions occurred after coronary angioplasty. Serious bleeding occurred in 7.6% of patients (37 of 488), predominantly at the catheterization entry site. There were 3 instances of central nervous system bleeding, 1 fatal. Fibrinogen levels declined to 83% of baseline at 24 hours. Weight-based dosing may explain the low incidence of serious bleeding in this study. The in-hospital mortality was 6.6% (32 of 488). This study documents that the dose of duteplase used in the International Study of Infarct Survival-3 results in a 90-minute coronary artery patency rate and safety profile comparable to those reported in published studies on the approved dose of alteplase.

Coronary Angiography↗