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Biomedical subjects

J D Rozich

Publications and source records attributed to J D Rozich.

13 recordsLinked to original sources
PubMed2003

Adverse drug event trigger tool: a practical methodology for measuring medication related harm.

Adverse drug events continue to be the single most frequent source of healthcare mishaps, continually placing patients at risk of injury. This is not unexpected, given that drug treatment is the most common medical intervention and medication use is a highly complex, multidisciplinary, and largely manual process. Assessing the actual safety of drug use has been historically difficult, mainly because traditional methods such as chart audits and voluntary reporting of data have been shown to be expensive, insensitive, and largely ineffective for detecting mistakes in drug administration and drug related adverse clinical events (ADEs). Computerized methods for detecting ADEs, employing sentinel words or "triggers" in a patient's medical record, are effective but expensive and require customized software linkage to pharmacy databases. This paper describes the use of the "trigger tool", a relatively low cost and "low tech" modification of the automated technique. The adapted technique appears to increase the rate of ADE detection approximately 50-fold over traditional reporting methodologies.

Adverse Drug Reaction Reporting Systems↗
PubMed2003

Methodology and rationale for the measurement of harm with trigger tools.

The growing recognition of harm as an unwelcome and frequently unrecognized byproduct of health care has initiated focused efforts to create highly reliable organizations for safe healthcare delivery. While debate continues over the exact magnitude of harm, there is a general acceptance of the need to improve our ability to deliver care in a safer manner. A major barrier to progress in safety has been the ability to effectively measure harm consistently and thus develop effective and targeted strategies to prevent its occurrence. This has resulted in a shift from initiatives focused exclusively on analysis of errors to those targeting events linked to harm. There is a growing recognition of a distinction between errors and adverse events as they often represent unique concepts fostering different strategies for improvement of safety. Conventional approaches to identifying and quantifying harm such as individual chart audits, incident reports, or voluntary administrative reporting have often been less successful in improving the detection of adverse events. As a result, a new method of measuring harm--the trigger tool--has been developed. It is easily customized and can be readily taught, enabling consistent and accurate measurement of harm. The history, application, and impact of the trigger tool concept in identifying and quantifying harm are discussed.

Health Services Research↗
PubMed1996

Basis for increased microtubules in pressure-hypertrophied cardiocytes.

BACKGROUND: We have shown the levels of the sarcomere and the cardiocyte that a persistent increase in microtubule density accounts to a remarkable degree for the contractile dysfunction seen in pressure-overload right ventricular hypertrophy. In the present study, we have asked whether these linked phenotypic and contractile abnormalities are an immediate and direct effect of load input into the cardiocyte or instead a concomitant of hypertrophic growth in response to pressure overloading. METHODS AND RESULTS: The feline right ventricle was pressure-overloaded by pulmonary artery banding. The quantity of microtubules was estimated from immunoblots and immunofluorescent micrographs, and their mechanical effects were assessed by measuring sarcomere motion during microtubule depolymerization. The biogenesis of microtubules was estimated from Northern and Western blot analyses of tubulin mRNAs and proteins. These measurements were made in control cats and in operated cats during and after the completion of right ventricular hypertrophy; the left ventricle from each heart served as a normally loaded same-animal control. We have shown that the alterations in microtubule density and sarcomere mechanics are not an immediate consequence of pressure overloading but instead appear in parallel with the load-induced increase in cardiac mass. Of potential mechanistic importance, both these changes and increases in tubulin poly A+ mRNA and protein coexist indefinitely after a new, higher steady state of right ventricular mass is reached. CONCLUSIONS: Because we find persistent increases both in microtubules and in their biosynthetic precursors in pressure-hypertrophied myocardium, the mechanisms for this cytoskeletal abnormality must be sought through studies of the control both of microtubule stability and of tubulin synthesis.

Animals↗
PubMed1995

Load effects on gene expression during cardiac hypertrophy.

Hemodynamic load is a primary regulator of cardiac mass. A potential proximal event in this regulatory pathway is thought to be the induction of immediate early genes, and markers of this process include the re-expression of genes for fetal sarcomeric proteins and the ventricular expression of atrial natriuretic factor (ANF). Previous in vivo models which have examined these questions have often neither quantified myocardial loading nor accounted for covariables which may affect gene expression such as the renin-angiotensin-aldosterone system, the sympathetic nervous system, or baroreceptors. Thus, whether load alone is sufficient to induce immediate early genes, which may ultimately result in cardiac hypertrophy, remains unknown. In the present study two models of right ventricular (RV) pressure overload were created by partially occluding the pulmonary artery (PA), either with a balloon catheter for 1 or 4 h, or with a surgically placed PA band for 12, 24, or 48 h. Serum catecholamine concentrations were determined in a subset of RV pressure overload cats at basal state, after 5 min of balloon inflation, and after 1 h of balloon inflation to examine the effects of this systemic trophic factor on IEG induction. Northern blot analysis for c-fos, egr-1, alpha-skeletal actin, and ANF from paired RV and left ventricular (LV) RNA allowed the effect of load (selectively increased in the RV) to be separated from other systemic variables (present in both ventricles). The relative signal intensities of the optical density of RV and LV mRNA autoradiograms were determined from northern blots, alternate lanes of which were loaded with 7.5 micrograms of total RNA from RV and LV tissue from the same cat. Partial PA occlusion caused RV systolic pressure to increase from a control value of 22 +/- 1 mmHg to 57 +/- 6 mmHg after 1 h, 59 +/- 5 mmHg after 4 h, and 58 +/- 5 mmHg after 48 h of RV pressure overload (RVPO). Serum norepinephrine and epinephrine levels at both 5 and 60 min of RVPO were not significantly different from basal levels. The RV/LV ratios of mRNA for both egr-1 and c-fos were equal in control and 48 h PA banded animals, but were increased in the 1 and 4 h balloon RVPO cats. The RV/LV ratio of mRNA for alpha-skeletal actin was equal in the basal state and did not increase after 12, 24, or 48 h of RVPO. After 48 h of RVPO, total RNA was increased in the RV compared with the LV (1.9 +/- 0.1 v 1.1 +/- 0.1 micrograms/g tissue, P < 0.05). ANF expression was present in the RV after 48 h of RVPO, but absent in same-animal LV and all control ventricles. Thus, while increased load alone did not alter the expression of alpha-skeletal actin, it was sufficient both to induce increased expression of two distinct classes of immediate early genes, as well as ANF, and to increase total RNA, indicating hypertrophic growth initiation.

Animals↗
PubMed1993

Rothia dentocariosa endocarditis complicated by perivalvular abscess.

A 35-year-old man with a history of intravenous drug use developed endocarditis due to Rothia dentocariosa that was complicated by a perivalvular abscess. Despite combined medical and surgical treatment, abscess formation progressed following aortic valve replacement, and the patient died during a second operative procedure. This is the sixth case of Rothia dentocariosa endocarditis reported in the English-language literature, and to our knowledge, the only case in which a perivalvular abscess has been documented.

Abscess↗
PubMed1993

Rapid expression of the Na(+)-Ca2+ exchanger in response to cardiac pressure overload.

This report identifies a rapid increase in the expression of cardiac Na(+)-Ca2+ exchanger mRNA in response to an acute pressure overload. This enhanced exchanger expression appeared within 1 h after the onset of right ventricular pressure overload in the cat and was sustained during cardiac overloading for at least 4 h. Maintenance of this right ventricular pressure overload for 48 h evoked an increase in the production of exchanger protein. Because of our previous finding that load imposition on the heart initiates cell growth and our hypothesis that this is in response to the enhanced entry of cellular cations, we then examined the effect of Na+ influx into cultured adult cardiac myocytes, or cardiocytes, in terms of early anabolic responses. Pressure overload of the heart and cardiocyte Na+ influx were found to produce a common, rapid result in terms of both enhanced Na(+)-Ca2+ exchanger expression and accelerated synthesis of general and contractile proteins, the hallmarks of cardiac hypertrophy.

Animals↗
PubMed1992

Endothelin stimulates multiple responses in isolated adult ventricular cardiac myocytes.

We have examined the responses to endothelin (ET) in isolated adult cardiac myocytes from both rodent and feline species to assess whether endothelin may have a role in the induction or mediation of cardiac hypertrophy in the adult animal. We have evidence that ET acts by more than one mechanism to promote cell-signaling events believed important in growth regulation. In isolated adult cardiac ventricular myocytes labeled overnight with [3H]inositol, endothelin (ET) promoted a two- to fourfold increase in the accumulation of inositol polyphosphates in a dose-dependent manner with an half-maximal effective concentration (EC50) of approximately 5 nM. In contrast, picomolar concentrations of ET promoted an increase in both the extent and velocity of sarcomere shortening in electrically stimulated myocytes. Pretreatment of cells with pertussis toxin had no effect on the ET-stimulated phosphoinositide hydrolysis, but blocked the ET-stimulated positive inotropic effect. In addition to these early responses to ET, results obtained by Northern blot analysis demonstrate that exposure of isolated cardiac myocytes to 100 nM ET promoted the expression of c-fos and c-zif in both mammalian species. These data demonstrate that ET stimulates multiple cell-signaling pathways in adult mammalian cardiac myocytes. A paracrine mechanism of regulation of adult myocardium is suggested.

Animals↗
PubMed1992

Mitral valve replacement with and without chordal preservation in patients with chronic mitral regurgitation. Mechanisms for differences in postoperative ejection performance.

BACKGROUND: Standard mitral valve replacement (MVR) in patients with chronic mitral regurgitation consistently results in a decrease in postoperative left ventricular (LV) ejection performance. This fall in ejection performance has been attributed, at least in part, to unfavorable loading conditions imposed by the elimination of the low-impedance pathway for LV emptying into the left atrium. In contrast to standard MVR in which the chordae tendineae are severed, however, MVR with chordal preservation (MVR-CP) does not usually decrease LV ejection performance despite similar removal of the low-impedance pathway. The purpose of the present study was to define the mechanisms responsible for this discordance in postoperative ejection performance between MVR with and without chordal preservation. METHODS AND RESULTS: Echocardiography and sphygmomanometer blood pressures were obtained in 15 patients with pure chronic mitral regurgitation before and 7-10 days after mitral valve surgery. These measurements were used to calculate ventricular volume, wall stress, and ejection fraction. Seven patients underwent MVR with chordal transection (MVR-CT), and eight patients underwent MVR-CP. MVR-CT resulted in no postoperative change in LV end-diastolic volume, a significant increase in LV end-systolic volume, a significant increase in end-systolic stress, from 89 +/- 9 to 111 +/- 12 g/cm2 (p < 0.05), and a significant decrease in ejection fraction, from 0.60 +/- 0.02 to 36 +/- 0.02 (p < 0.05). In contrast, patients who underwent MVR-CP had a significant decrease in LV end-diastolic and end-systolic volumes. End-systolic wall stress actually fell from 95 +/- 6 to 66 +/- 6 g/cm2 (p < 0.05), and ejection fraction was unchanged (0.63 +/- 0.01 before and 0.61 +/- 0.02 after mitral valve surgery) instead of reduced. CONCLUSIONS: MVR-CT resulted in a decrease in ejection performance caused in part by an increase in end-systolic stress, which in turn increased end-systolic volume. Conversely, MVR-CP resulted in a smaller LV size, allowing a reduced end-systolic stress and preservation of ejection performance despite closure of the low-impedance left atrial ejection pathway.

Chordae Tendineae↗
PubMed1991

Dialysis-induced alterations in left ventricular filling: mechanisms and clinical significance.

Quantitative two-dimensional (2-D) and Doppler echocardiography were used to determine whether hemodialysis results in alterations in left ventricular (LV) diastolic filling that might contribute to dialysis-induced hypotension, as well as to assess whether any hemodynamic variables or indices of diastolic filling might be used to identify which patients were at the greatest risk of becoming hemodynamically unstable during dialysis. Sixteen male patients undergoing routine maintenance hemodialysis for end-stage renal disease were prospectively studied before and after hemodialysis. Following hemodialysis there was a significant prolongation (P less than 0.05) in LV isovolumetric relaxation time (IVRT), as well as a significant reduction in the rate and extent of early rapid ventricular filling (P less than 0.005); in contrast, late atrial-assisted filling did not change significantly. A multiple stepwise linear regression analysis of predialysis hemodynamic parameters and noninvasive indices of LV filling showed that there was a significant independent inverse relationship between the frequency of dialysis-related hypotensive episodes and the duration of early LV filling (r = -0.81; P less than 0.001). These results suggest that hemodialysis results in discrete alterations in early LV filling, with no significant compensatory increase in late atrial-assisted ventricular filling. Further, patients with the shortest early LV filling times appeared to have the greatest predilection for becoming hemodynamically unstable during dialysis.

Aged↗
PubMed1989

Reversion of mitral valve preclosure in acute aortic insufficiency secondary to infective endocarditis.

A 59-year-old man presented with culture-negative endocarditis. Serial echocardiographic/Doppler studies disclosed progressive aortic insufficiency with resultant premature closure of the mitral valve. At the time the patient developed PMVC he was considered for emergent aortic valve replacement; ultimately, however, he was deemed inoperable because of his underlying medical problems. Surprisingly, the patient gradually improved on antibiotic therapy alone, with subsequent hemodynamic stabilization and reversion of the PMVC. This case represents the first description of reversion of PMVC in a medically treated patient with severe aortic insufficiency secondary to infective endocarditis, and underscores the importance of basing management decisions concerning aortic valve replacement in infective endocarditis upon the entire constellation of clinical findings rather than a single echocardiographic sign.

Aortic Valve Insufficiency↗
PubMedDate not supplied

Physician-owned imaging centers: the future is now.

Although changes in the health care arena have made inroads in physicians' autonomy and reimbursement, new opportunities have also emerged. We describe basic principles that can help develop freestanding, independent, physician-owned imaging centers offering cost-competitive, high-quality services. To succeed, physicians must invest in their companies, think strategically, pursue clear objectives, examine data and be willing to assume a certain amount of risk. Marketing their services is critically important and requires careful attention to patients and referring physicians. We have found that, while these challenges are large, the rewards are substantial.

Ambulatory Care Facilities↗