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Biomedical subjects

S M Jafri

Publications and source records attributed to S M Jafri.

At least 37 records · Page 2Linked to original sources
PubMed1992

Factors influencing platelet serotonin uptake in essential hypertension.

In a study of the mechanism(s) of platelet serotonin uptake alteration in essential hypertension, a total of 90 blood samples were analysed for platelet count and platelet serotonin uptake. These included 20 blood samples each of hypertensives, controls before and after cross-incubation experiments and 10 samples of hypertensives after control of blood pressure. It was observed that serotonin uptake was markedly reduced in hypertensive platelets. Diminished serotonin uptake in essential hypertension correlated directly with diastolic and mean arterial blood pressure and inversely with plasma total cholesterol values. In cross-incubation experiments using control platelets and hypertensive plasma, there was a significant reduction in platelet serotonin uptake (303.06 +/- 86.28 cpm/10(8) vs. 204.26 +/- 66.45 cpm/10(8); P less than 0.001), whereas hypertensive platelets when incubated with control plasma, showed increased serotonin uptake (233.50 +/- 75.19 cpm/10(8) vs. 312.64 +/- 79.54 cpm/10(8); P less than 0.01). Upon control of blood pressure, the platelet serotonin uptake improved significantly (205.45 +/- 70.0 cpm/10(8) vs. 266.77 +/- 61.68 cpm/10(8); P less than 0.05-0.01). From these results, it appears that reduced platelet serotonin uptake in essential hypertension is a reversible phenomenon probably governed by the presence of plasma factor(s) and/or altered platelet-membrane function.

Adult↗
PubMed1992

Testotoxicosis: gonadotrophin-independent male sexual precocity.

In this era of rapidly developing investigational tools and pharmacology, the pathophysiology of precocious puberty is becoming well defined. What was previously thought to be a form of gonadotrophin releasing hormone (GNRH)-dependent central precocious puberty is now classified as GNRH-independent familial testotoxicosis. We present two such cases and review the clinical features, pathophysiology and treatment of testotoxicosis.

Child↗
PubMed1992

Transesophageal echocardiographic findings in patients with orthotopic heart transplantation.

This study was performed to determine the diagnostic value of TEE in recipients of orthotopic heart transplantation. Findings on TEE were compared with those of TTE in 30 patients with orthotopic heart transplantation. Transesophageal echocardiography identified left atrial appendage and flow across the interatrial septum ... findings not detected by TTE. In addition, pronounced bulging of the interatrial septum was seen in six patients by TEE and not by TTE. Spontaneous echo contrast (smoke) in the atria was detected by TEE in 14 patients and by TTE in one patient. Abnormal geometry of the atria and donor-recipient atrial anastomosis was identified in all patients by TEE and TTE. Our findings suggest that TEE should be selectively utilized in the operating room, in patients with suspected atrial thrombi, and in those with clinically significant right ventricular volume overload to assess integrity of interatrial anastomosis.

Echocardiography↗
PubMed1992

Temporary transvenous cardiac pacing.

Temporary cardiac pacing in the critical care setting can be a lifesaving intervention in a number of clinical situations. A variety of catheter types and pulse generators are available. Insertion techniques include the use of fluoroscopic imaging, intracavitary ECG monitoring, and blind advancement with surface ECG monitoring. This article focuses on the indications, equipment, techniques, complications, and troubleshooting of temporary transvenous cardiac pacemakers.

Cardiac Pacing, Artificial↗
PubMed1991

Medical therapy after acute myocardial infarction.

Several therapeutic agents have been tested for secondary prevention after acute myocardial infarction. Each patient presents a clinical challenge and gives the physician an opportunity to use the tests and therapy most likely to benefit the clinical course. The presence of other associated medical conditions, the type of myocardial infarction, the presence or absence of accompanying ischemia, left ventricular dysfunction, intracardiac thrombus, or ventricular arrhythmias dictate the choices that are to be made. It is apparent from this review that no single class of agents can be considered a cure, although beta-adrenergic blocking agents come the closest to this role. Analysis of these drugs helps individualize drug therapy and provides a physiologic probe to understanding the pathophysiologic processes that characterize the period after myocardial infarction. To address the impact of developing technology and drug availability on the practice and cost of medical care, the American College of Cardiology and the American Heart Association have developed guidelines for the management of patients with myocardial infarction. The clinical trial remains the best test for the assessment of therapeutic choices and can also expand our knowledge of the natural history of the disease process. Nevertheless, the issue of appropriate therapy is ever-changing, affected by the explosion of new technology and the continued investigation into the pathophysiology of coronary artery disease.

Adrenergic beta-Antagonists↗
PubMed1990

Effects of cigarette smoking and propranolol in survivors of acute myocardial infarction.

The effect of propranolol on mortality and reinfarction after acute myocardial infarction (AMI) in cigarette smokers and nonsmokers was studied in the Beta Blocker Heart Attack Trial. Cigarette smokers (n = 2,332) were 5 years younger than nonsmokers and had a lower incidence of diabetes mellitus, systemic hypertension, previous AMI and cardiomegaly. Among cigarette smokers, the placebo group had a higher total mortality rate than the propranolol group (11.0 vs 7.4%, p less than 0.0008) and more sudden cardiac deaths (7.1 vs 4.6%, p less than 0.009). In nonsmokers the placebo group had a mortality (7.9 vs 7.1%, p greater than 0.64) similar to the propranolol group. After baseline adjustment, cigarette smokers were estimated to have 1.6 times the risk of dying as compared to nonsmokers (p less than 0.0007). Adjusting for baseline differences, both treatment with propranolol and nonsmoking were predictors of survival. No detectable nonsmoking/propranolol interaction could be identified. In survivors of AMI a beneficial effect of propranolol is observed for cigarette smokers. Nevertheless, cigarette smoking continues to be a risk factor for mortality after AMI even for those receiving propranolol.

Double-Blind Method↗
PubMed1990

Left ventricular diastolic function in sepsis.

Although systolic dysfunction of the left ventricle has been characterized in septic shock (SS) and sepsis without shock (SWS), diastolic abnormalities are less well characterized. Diastolic filling was determined using pulsed Doppler transmitral spectral tracings in 13 patients with SS, ten patients with SWS, and 33 normal controls. Diastolic filling variables and heart rate were similar in patients with SS and SWS. The SS and SWS patients had an abnormal pattern of diastolic filling compared with controls and were characterized by an increase in peak atrial velocity (70 +/- 20 cm/sec SS, 84 +/- 18 cm/sec SWS vs. 56 +/- 11 cm/sec controls, p less than .05), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.3, SS, 1.1 +/- 0.2 SWS vs. 1.5 +/- 0.4 controls, p less than .05), increased atrial filling fraction (39 +/- 11 SS, 42 +/- 6 SWS vs. 30 +/- 10 controls, p less than .05) and prolongation of atrial filling period as a function of the diastolic filling period (0.48 +/- 0.10 SS, 0.43 +/- 0.10 SWS vs. 0.30 +/- 0.07 controls, p less than .05). Heart rate was higher in SS and SWS compared with controls (116 +/- 15 beat/min SS, 110 +/- 26 beat/min SWS vs. 73 +/- 12 beat/min controls, p less than .05). In patients with SS and SWS, there is increased reliance on atrial systolic contribution to diastolic filling. We conclude that diastolic dysfunction occurs with systemic infections.

Adult↗
PubMed1990

Acute neurohormonal and hemodynamic response to a new peak III phosphodiesterase inhibitor (ICI 153,110) in patients with chronic heart failure.

Peak III phosphodiesterase (PDE) inhibitors have combined positive inotropic and vasodilator effects. We studied 10 patients with chronic heart failure during and after infusion of intravenous (i.v.) ICI 153,110, an investigational peak III PDE inhibitor. Maximum hemodynamic response for the group occurred after cessation of infusion at a lower plasma drug concentration. At maximum hemodynamic response, cardiac index (CI) increased (2.4 +/- 0.5 vs. 3.2 +/- 0.37 L/min/m2, p less than 0.05) with a decrease in mean arterial pressure (MAP 91 +/- 5 vs. 80 +/- 3 mm Hg, p less than 0.05), pulmonary capillary wedge pressure (PCWP 25 +/- 2 vs. 17 +/- 3.1 mm Hg, p less than 0.01), systemic vascular resistance (SVR 1,422 +/- 106 vs. 983 +/- 97 dynes.s.cm-5, p less than 0.05) and pulmonary vascular resistance (PVR 227 +/- 39 vs. 16 +/- 31 dynes.s.cm-5, p less than 0.05). During the infusion, plasma renin activity (PRA) decreased from 6.34 +/- 2.53 to 3.6 +/- 3 ng/ml/h (NS). The five patients with high baseline PRA had a significant decrease (11.2 +/- 2.5 vs. 5.4 +/- 1.67 ng/ml/h, p less than 0.01) that preceded changes in CI and SVR by 1-2 h. These data suggest that reduction in PRA may have contributed to the hemodynamic effects of this peak III PDE inhibitor.

Dihydropyridines↗
PubMed1990

Obstructive jaundice: an unusual presentation of amoebic liver abscess.

A case of amoebic liver abscess with obstructive jaundice is described. Treatment with metronidazole resulted in improved general condition while the jaundice continued to increase. The abscess was twice aspirated and a total of 500 ml fluid was obtained with no improvement in the jaundice. A percutaneous catheter was introduced and drained 300-400 ml bile a day, decreasing and stopping over a week. The jaundice progressively improved.

Cholestasis↗
PubMed1987

Efficacy of propranolol therapy after acute myocardial infarction related to coronary arterial anatomy and left ventricular function.

The effect of the beta-adrenergic blocking agent propranolol on morbidity and mortality risk after acute myocardial infarction was studied relative to coronary anatomy and left ventricular (LV) ejection fraction in a subset of 406 patients participating in a randomized study of 3,837 patients in the Beta Blocker Heart Attack Trial (BHAT). Median follow-up for this subset of patients was 28 months. The mortality rate was 2% (2 of 100) in patients with 2- and 3-vessel coronary artery disease taking propranolol and 10% (12 of 126) in those taking placebo (p less than 0.02). In patients with 2- and 3-vessel coronary artery disease with decreased LV function (defined as ejection fraction less than 50%), no patient taking propranolol died, whereas 17% (7 of 42) taking placebo died (p less than 0.04). The salutary effect of propranolol on mortality in the larger BHAT after acute myocardial infarction also was evident in this population studied in regard to their coronary and LV anatomy and function.

Coronary Vessels↗
PubMed1987

Hemodynamic, pharmacokinetic and clinical response to CI-930 in congestive heart failure due to ischemic or dilated cardiomyopathy.

CI-930, a new type III phosphodiesterase inhibitor, was evaluated for treatment of refractory congestive heart failure. The hemodynamic, pharmacokinetic and clinical response to the drug was determined in 10 patients. At the peak plasma concentration after intravenous CI-930, cardiac index increased from 2.0 to 2.7 liters/min/m2 (p less than 0.002), pulmonary artery wedge pressure decreased from 26 to 17 mm Hg (p less than 0.001) and systemic vascular resistance decreased from 1,999 to 1,471 dynes cm-5 (p less than 0.05). Heart rate and blood pressure did not change significantly. Similar changes were observed with oral CI-930. Peak CI-930 plasma concentration occurred 1.2 +/- 0.8 hours after oral administration. Beneficial hemodynamic effects were sustained 12 to 18 hours after the oral dose. The sustained hemodynamic effects observed after oral administration appear to be related to an active metabolite of CI-930 that has prolonged duration of action and slow washout. The drug was well tolerated and has potential for treatment of congestive heart failure.

Administration, Oral↗
PubMed1987

Acute and chronic hemodynamic effects of nicardipine hydrochloride in patients with heart failure.

Acute and chronic hemodynamic effects at rest and during exercise of a new dihydropyridine calcium antagonist, nicardipine hydrochloride, were studied in 10 patients with chronic heart failure. Acute intravenous administration of nicardipine resulted in a significant decrease in arterial blood pressure, systemic vascular resistance, and pulmonary capillary wedge pressure. There was a significant increase in cardiac index, stroke volume index, and the left ventricular stroke work index. Cardiac index measured at peak exercise increased significantly when compared with the cardiac index obtained at peak exercise before the infusion. After 9 days of continuous therapy with nicardipine, 30 mg three times a day, a significant decrease in arterial blood pressure and systemic vascular resistance and a significant increase in the cardiac index, stroke volume index, and left ventricular stroke work index at rest were observed in response to a single oral dose of 30 mg nicardipine. Data at peak exercise were also obtained before and 2 hours after the oral administration of nicardipine. With this comparison there was a significant increase in cardiac index, stroke work index, and exercise duration. It is concluded that in this group of patients with severe chronic heart failure, nicardipine enhanced myocardial performance during rest and exercise and this enhancement is sustained after 9 days of oral therapy.

Administration, Oral↗
PubMed1986

Hemodynamic effects of a new type III phosphodiesterase inhibitor (CI-914) for congestive heart failure.

Hemodynamic response after intravenous and oral administration of a new phosphodiesterase inhibitor, CI-914, was studied in 13 patients with severe congestive heart failure. Comparable significant increases in cardiac index of 26% (p less than 0.01) and 19% (p less than 0.02) after intravenous and oral administration were observed. Systemic vascular resistance, right atrial and pulmonary artery wedge pressure decreased significantly after intravenous drug administration. Although similar changes occurred after oral administration, they were not statistically significant. Peak CI-914 plasma concentration occurred 2.3 +/- 2.2 hours after oral drug administration and exhibited measurable hemodynamic effects for up to 10 to 12 hours. Seven of the 13 patients received long-term oral CI-914 for as long as 12 weeks and exhibited an improvement in New York Heart Association functional class and exercise capacity. Five patients died with progressive heart failure, 1 patient died suddenly and 1 died of sepsis. The drug was well tolerated and appears to have potential as a cardiotonic agent.

Administration, Oral↗