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Biomedical subjects

Y Rozenman

Publications and source records attributed to Y Rozenman.

At least 91 records · Page 5Linked to original sources
PubMed1993

Arterial remodelling after percutaneous transluminal balloon angioplasty.

Atheromatous coronary artery disease progresses by atheroma accretion, plaque rupture and thrombus formation, with or without spontaneous fibrinolysis. The natural history may be altered by modifying risk factors in an attempt to induce regression, or treated by mechanical means such as balloon angioplasty, directional coronary atherectomy or drills, or flow modulated by the insertion of an aorto coronary bypass graft with or without endarterectomy. Here we discuss the natural history of the atheromatous disease in a series of 355 patients who underwent at least one PTCA procedure and then underwent a second angiographic study to determine the changes in the dilated and nondilated arteries.

Angioplasty, Balloon, Coronary↗
PubMed1992

Angiographic findings in the coronary arteries after thrombolysis in acute myocardial infarction.

The angiographic appearance of the coronary arteries was examined in 308 patients with acute myocardial infarction (AMI) who received high-dose intravenous thrombolytic therapy. Coronary angiography was performed on day 7 after admission to the hospital. Patients had an average of 2.4 discrete arterial narrowings or obstructions. The narrowings were proximal and related to bifurcations. Four fifths of the culprit arteries were patient; 104 (34%) had a ruptured plaque, 22 (7%) had an ulcerated plaque, and in 190 (62%) the lesions were eccentric. Patients differed from a comparable, previously studied, control series of 302 patients with chronic stable angina pectoris who had more extensive disease. They had 5.7 narrowings/patient, also located proximally and at bifurcations, but more widely distributed in the coronary tree. Patients with AMI who are suitable for thrombolysis have a unique coronary angiographic picture. The data confirm that AMI is caused by sudden rupture of a localized atheromatous plaque that initiates an obstructive thrombotic cascade.

Angina Pectoris↗
PubMed1991

Ion-pairing high-performance liquid chromatographic method for the determination of 5-aminosalicylic acid and related impurities in bulk chemical.

An ion-pairing high-performance liquid chromatographic method has been developed for the determination of 5-aminosalicylic acid (5-ASA) bulk chemical in the presence of thirteen potential synthetic process impurities. In addition, the method is suitable for the determination of the in process intermediate, 5-nitrosalicylic acid. A selective method was achieved on a Hypersil-BDS reversed-phase column using 1-heptanesulfonic acid sodium salt as the ion-pairing reagent in a 0.08 M sodium phosphate buffer (pH 2) containing 0.005 M 1-heptanesulfonic acid sodium salt and 0.07 M sodium chloride-methanol-tetrahydrofuran (85:11:4, v/v/v) isocratic mobile phase. The method was validated using a multi-day, intra-laboratory protocol. The validation addressed linearity, accuracy, precision, sensitivity, and ruggedness of the method. The validated method characterizes the purity of 5-ASA bulk chemical.

Aminosalicylic Acids↗
PubMed1991

Magnetic resonance imaging with superparamagnetic iron oxide particles for the detection of myocardial reperfusion.

The effect of superparamagnetic iron oxide particles on magnetic resonance myocardial signal intensity was examined in order to define the ability of this agent to identify normal, ischemic, and reperfused myocardium. Data were obtained from 6 normal rats (group 1) and from 6 heterotopic isogenic rat heart transplants (group 2) at 4.7 T with a multislice spin-echo sequence. Images were acquired in (a) normal rats before and after the infusion of 36 mumol Fe/kg of AMI-25 (group 1) and (b) rat heart transplants during control, global myocardial ischemia (before and after the injection of 72 mumol Fe/kg of AMI-25), and following reperfusion (group 2). Myocardial signal intensity decreased by 36 +/- 4%, p less than 0.001, following contrast infusion in normal hearts (group 1). The intensity remained constant in the rat heart transplants (group 2) during coronary occlusion, both before and after the infusion of AMI-25 and decreased by 61 +/- 7%, p less than 0.001, upon reperfusion. The larger effect of AMI-25 in reperfused as compared to normal myocardium suggests the presence of ischemia-induced hyperemia. There was no significant difference (analysis of variance) among intensities from different myocardial regions in either group at any stage of the experiment. We conclude that the use of AMI-25 permits identification of normal, ischemic, and reperfused myocardium and may therefore be helpful for the early detection of reperfusion following thrombolytic therapy for acute myocardial infarction.

Animals↗
PubMed1990

Heterotopic transplanted rat heart: a model for in vivo determination of phosphorus metabolites during ischemia and reperfusion.

A model of heterotopic isogenic rat heart transplantation was developed in order to noninvasively observe the acute and chronic metabolic changes of ischemia. This study presents the results of 31P spectroscopy during acute global ischemia and reperfusion. The advantages of this model over other surface coil in vivo ischemia experiments are: (1) Thoracotomy for surface coil positioning is not required, thus the results are not influenced by the effect of recent major surgery. (2) Survival is not influenced by the degree of ischemic damage to the transplant, and the model enables repeated long-term studies of the metabolic effect of reversible ischemia, and myocardial infarction. (3) The pathologic process created is homogeneous and thus the results are not complicated by variation in the severity of myocardial ischemia.

Animals↗
PubMed1990

Cardiovascular MR imaging with iron oxide particles: utility of a superparamagnetic contrast agent and the role of diffusion in signal loss.

This study describes the effect of superparamagnetic iron oxide on myocardial signal intensity and defines the mechanism of action of this agent. Magnetic resonance images of the heart and relaxation data were obtained in 19 rats, and another three rats were used for measurements of contrast material concentration in the heart, with the contrast agent enriched with iron-59. A dose of 36 mumols of iron per kilogram induced homogeneous signal loss in the myocardium with a gated spin-echo sequence with a repetition time of 1,500 msec and an echo time of 20 msec. The reduction in signal intensity was the result of a combination of diffusion-dependent and diffusion-independent T2 shortening. The diffusion effect results from dephasing of spins moving across magnetic field gradients generated in the tissue by the contrast agent. The relative contribution of the diffusion-induced signal loss observed in vivo was larger than that predicted from the in vitro relaxation measurements. The reduced in vitro effect is likely the result of loss of a portion of the intramyocardial blood volume during sample preparation, as assessed with the Fe-59 measurements.

Animals↗
PubMed1989

Contact lens-related deep stromal neovascularization.

We observed five eyes (five patients) with deep stromal neovascularization and scarring in patients wearing soft contact lenses during a six-month period. There was no evidence suggestive of other causes of interstitial keratitis. Two patients were aphakic and required a penetrating keratoplasty. Deep stromal vascularization must be added to the growing list of visually significant soft contact lens complications, and soft lens wear should be considered in the differential diagnosis of deep stromal neovascularization.

Adult↗
PubMed1987

Chronotropic effect of hydralazine and its mechanism of symptomatic sinus bradycardia.

The positive chronotropic effect of hydralazine was studied in 9 patients with symptomatic sinus bradycardia. Hydralazine was given in an intravenous dose of 0.15 mg/kg and heart rate, blood pressure, sinoatrial conduction time (Narula method) and corrected sinus node recovery time were measured. The effect of hydralazine was also studied after total autonomic nervous system blockade using 0.04 mg/kg of atropine and 0.2 mg/kg of propranolol intravenously. In the control state hydralazine produced an increase of 28 +/- 15% (mean +/- standard deviation) in heart rate, and this was essentially due to a decrease in sinoatrial conduction time (by 32 +/- 32%, p less than 0.05). Corrected sinus node recovery time also tended to shorten (decrease of 21 +/- 34%, difference not significant). After total autonomic blockade intrinsic heart rate did not change or increased very little (9 +/- 14%) after administration of hydralazine and there was no consistent change in sinoatrial conduction and corrected sinus node recovery times. The small residual effect of hydralazine on heart rate was related to incomplete autonomic blockade, since the effect of postural change (standing) on heart rate was also not totally abolished. The study showed that the positive chronotropic effect of hydralazine was mainly due to a change in sinoatrial conduction with a smaller change in corrected sinus node recovery time, and the major chronotropic effect of the drug was mediated by the autonomic nervous system.

Aged↗
PubMed1987

Detection of varicella-zoster virus nucleic acid in neurons of normal human thoracic ganglia.

Tissue sections from four normal human thoracic ganglia were hybridized in situ with a varicella-zoster virus-RNA probe. Varicella-zoster virus was detected in two of four ganglia, localized exclusively in neurons. The detection of latent varicella-zoster virus genetic material in thoracic ganglia provides further evidence of varicella-zoster virus latency at multiple levels of the human neuraxis and supports the notion that the neuron is the primary site of herpesvirus latency.

DNA, Viral↗
PubMed1987

Left ventricular function during physiological cardiac pacing: relation to rate, pacing mode, and underlying myocardial disease.

The hemodynamic effects of cardiac pacing at different rates and in different modes were studied in 21 patients who were candidates for permanent pacemaker implantation. Nine of these had primary conduction disturbances (PCD), ten had ischemic heart disease (IHD), seven with additional cardiac failure (CHF), and two had hypertrophic cardiomyopathy (HCM). In patients with PCD, atrial (AOO) and AV sequential (DVI) pacing did not change systolic blood pressure and pulse pressure but ventricular (VVI) pacing caused a progressive fall in these measurements, especially as heart rate increased. Ventricular volume and stroke volume (counts) derived from radionuclide ventriculography (RVG) decreased progressively with higher pacing rates, especially during VVI pacing. Cardiac output was maintained during VVI pacing by the increase in heart rate; during AOO and DVI pacing, cardiac output increased. Similar but more marked differences were observed in patients with IHD and CHF and the changes were even greater in the patients with HCM. Left ventricular (LV) ejection fraction changed little with increasing heart rate in PCD but decreased progressively with the onset of ischemia in IHD and CHF. There was no difference in ejection fraction in the different pacing modes. Graphs related to LV contractility (end-systolic pressure-volume relations) showed that AOO pacing produced the highest and VVI pacing produced the lowest curves of myocardial contractility in all patient groups, except that at higher rates the AOO curve shifted down again in patients with IHD and CHF, presumably with the onset of myocardial ischemia. This study showed that physiological pacing produced the best hemodynamic results in all patient groups. Higher pacing rates should be avoided in patients with ischemic heart disease while VVI pacing should not be used in patients with HCM. Blood pressure and RVG studies during temporary pacing are useful in selecting the optimal pacing system in an individual patient when the clinical choice is not clear.

Bradycardia↗
PubMed1986

Radionuclide left ventricular function curve during atrial pacing in normal subjects and in patients with coronary artery disease.

We used radionuclide angiography during right atrial pacing to assess left ventricular function in 7 normal subjects and 20 patients with coronary artery disease. A left ventricular function curve relating stroke volume to end-diastolic volume was plotted for each patient. The normal pacing ventricular function curve was a straight line passing through the origin of axes. The pacing ventricular function curve was abnormal in 18 of the 20 patients with coronary artery disease, and three different shaped curves were obtained, reflecting decreased contractile force for the same end-diastolic volume during ischemia. Cardiac output and blood pressure do not change during atrial pacing, thus the Frank-Starling relationship is evaluated by this method during almost experimentally controlled conditions. Relating stroke volume to end-diastolic volume, and not end-diastolic pressure, distinguishes between overall left ventricular systolic function and left ventricular compliance.

Adult↗
PubMed1986

Left ventricular function in acute myocardial infarction: assessment by nuclear angiography.

Left ventricular function was assessed in 38 patients two to six days after acute myocardial infarction using nuclear angiocardiography and the following parameters were measured: Left ventricular end-diastolic (LVEDV) and end-systolic volumes (LVESV), ejection fraction (LVEF), indices of left ventricular filling and emptying, right ventricular ejection fraction and ejection rate. Their clinical significance was assessed by their relationship to the patients site and size of infarction, functional capacity, morbidity and mortality. The most sensitive indices of depressed left ventricular function were the EF and ESV. Thus, function was preserved in patients with a small inferior infarction (LVEF = 0.57 +/- 0.07, LVESV = 69 +/- 14 ml) and in Killip Class I (LVEF = 0.48 +/- 0.13, LVESV = 80 +/- 20 ml). Function was disturbed most in patients with extensive anterior infarction (LVEF = 0.18 +/- 0.12, LVESV = 131 +/- 46 ml), Killip Class IV (LVEF = 0.13 +/- 0.07, LVESV = 160 +/- 35 ml), cardiogenic shock (LVEF = 0.14 +/- 0.07, LVESV = 160 +/- 35 ml), pulmonary edema (LVEF = 0.11 +/- 0.06, LVESV = 166 +/- 25 ml) and pulmonary capillary wedge pressure greater than 20 mm Hg (LVEF = 0.14 +/- 0.07, LVESV = 160 +/- 33 ml). Previous infarction was associated with LV dilatation and a greater LVEDV. A lower ejection fraction signified a large infarct and poor left ventricular function. If the ejection fraction was less than 0.15, the patients were unlikely to leave the hospital alive, or if less than 0.25, they were left with poor residual ventricular function and either had significant cardiac failure or high late mortality. Nuclear angiocardiography was a simple method of predicting the clinical pattern and prognosis in each patient and emphasized the importance of limiting infarct size in acute myocardial infarction.

Adult↗
PubMed1985

Prevention of myocardial damage in acute myocardial ischemia by early treatment with intravenous streptokinase.

We evaluated the effectiveness of early intravenous administration of 750,000 units of streptokinase in 53 patients with acute myocardial ischemia treated by a mobile-care unit at home (9 patients) or in the hospital (44 patients). Treatment was begun an average (+/- S.D.) of 1.7 +/- 0.8 hours from the onset of pain. Non-Q-wave infarctions developed subsequently in eight patients, whereas all the others had typical Q-wave infarct patterns. In 81 per cent of the patients the infarct-related artery was patent at angiography performed four to nine days after admission. Vessel patency was independent of the time of treatment, but residual left ventricular function was time dependent. Patients treated less than 1.5 hours after the onset of pain had a significantly higher ejection fraction (56 +/- 15 vs. 47 +/- 14 per cent; P less than 0.05) and infarct-related regional ejection fraction (51 +/- 19 vs. 34 +/- 20 per cent; P less than 0.01) and a lower QRS score (5.6 +/- 4.9 vs. 8.6 +/- 5.5; P less than 0.01) than patients receiving treatment between 1.5 and 4 hours after the onset of pain. Patients treated earlier by the mobile-care unit also had better-preserved left ventricular function than patients treated in the hospital. We conclude that thrombolytic therapy with streptokinase is most effective if given within the first 1.5 hours after the onset of symptoms of acute myocardial infarction.

Adult↗
PubMed1985

Heart rate influence on the systolic gradient across the stenotic aortic valve: theoretical evaluation and implications.

Peak systolic gradient across the aortic value, measured invasively or noninvasively is used in many laboratories for estimation of the severity of the stenosis (= actual valve area). This study shows that when cardiac output is normal the gradient across the valve is influenced by heart rate (HR) apart from valve area. A rate-corrected peak systolic gradient (PSGc) is defined by the formula (formula; see text) and its importance for clinical decision making is demonstrated. The significance of bradycardia in the pathogenesis of syncope in aortic stenosis is discussed.

Aortic Valve Stenosis↗
PubMed1985

Treatment of ocular inflammation with diclofenac sodium: double-blind trial following cataract surgery.

A controlled trial of diclofenac sodium was carried out in 100 patients undergoing intracapsular cataract extraction. All patients were treated with dexamethasone eyedrops twice daily, plus either diclofenac sodium 50 mg tid or matching placebo tid, started 24 hours before surgery and continued for four weeks. In comparison with those in the placebo group, patients in the diclofenac group showed significant decreases in most signs of ocular inflammation. Diclofenac therapy was well tolerated, except in one patient, and may safely be used to reduce intraocular inflammation.

Aged↗
PubMed1985

Painful bullous keratopathy following pediatric cataract surgery with intraocular lens implantation.

A child with a history of a monocular congenital cataract, cataract surgery and intraocular lens implantation at age three developed pseudophakic bullous keratopathy which persisted following intraocular lens removal and vitrectomy two years later. At age nine she presented to the Cornea Service at Wills Eye Hospital with painful bullous keratopathy and underwent a penetrating keratoplasty and anterior vitrectomy. The case is presented to bring attention to potential long-term corneal complications of pediatric cataract surgery with intraocular lens implantation.

Cataract Extraction↗