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Biomedical subjects

R P Bauman

Publications and source records attributed to R P Bauman.

At least 19 recordsLinked to original sources
PubMed1999

Coronary artery restenosis after atherectomy is primarily due to negative remodeling.

The primary cause of restenosis following directional coronary atherectomy (DCA) remains obscure. "Negative remodeling," a decrease in vessel area, is believed to be more causative than is increase in plaque area. The DCA technique used in these patients, designed to facilitate the removal of plaque, should allow a more precise evaluation of the relative roles of these two mechanisms. Twenty-five patients underwent DCA. In 17, complete angiographic and intravascular ultrasound (IVUS) images were obtained before and after DCA and at follow-up (6 to 9 months). Internal elastic lamina (IEL), lumen, and plaque areas were calculated at preatherectomy, postatherectomy, and follow-up. Postatherectomy, the mean IEL area increased by 32% and the mean plaque area decreased by 51%, resulting in a significant mean increase in lumen area, 500%. At follow-up when compared to postatherectomy, the change in IEL area was variable; however, the mean did not change significantly (p = 0.58). Plaque area change, when standardized for initial vessel size, was small (mean increase 2.8 +/- 3.5%). The mean lumen area did not decrease significantly at follow-up (p = 0.43). A highly significant correlation (r = 0.96) was noted between IEL area change and lumen area at follow-up. In contrast, the correlation between plaque area change and lumen area change over the same period was much less significant (r = 0.64). These data indicate that decrease in IEL area primarily is responsible for restenosis.

Atherectomy, Coronary↗
PubMed1998

Myocardial blood flow in awake dogs with chronic tricuspid regurgitation.

The primary purpose of this study was to define regional blood flow in dogs with chronic tricuspid regurgitation (TR) in order to determine if the marked hypertrophy of the right atria resulted in compromised myocardial perfusion. Myocardial blood flow (ml/min/gm) was measured with radiolabeled microspheres in eight dogs with TR during rest, moderate exercise (5 dogs), and infusion of adenosine (1 mg/kg/min), an index of minimal vascular resistance. Similar measurements were obtained in eight normal dogs. In TR, the ratio of right atrium (RA) and right ventricle (RV) to body weight was greater than in normal dogs, 77% and 30%, respectively. During rest, flow in the RA appendage was less than in nonappendage region in the normal dogs; no differences were noted in TR dogs, indicating an augmented hemodynamic role of the appendage in TR. Both RA and RV blood flow was greater in TR during rest but no other differences in flow were found between the two groups. Minimum vascular resistance in RV but not RA was slightly increased in TR versus normal. During marked myocyte hypertrophy, the vasculature of RA develops sufficiently to provide the same flow capacity as in the normal heart.

Adenosine↗
PubMed1998

Myonecrosis after revascularization procedures.

The detection of elevated cardiac enzyme levels and the occurrence of electrocardiographic (ECG) abnormalities after revascularization procedures have been the subject of recent controversy. This report represents an effort to achieve a consensus among a group of researchers with data on this subject. Creatine kinase (CK) or CK-MB isoenzyme (CK-MB) elevations occur in 5% to 30% of patients after a percutaneous intervention and commonly during coronary artery bypass graft surgery (CABG). Although Q wave formation is rare, other ECG changes are common. The rate of detection is highly dependent on the intensity of enzyme and ECG measurement. Because most events occur without the development of a Q wave, the ECG will not definitively diagnose them; even the ECG criteria for Q wave formation signifying an important clinical event have been variable. At least 10 studies evaluating > 10,000 patients undergoing percutaneous intervention have demonstrated that elevation of CK or CK-MB is associated not only with a higher mortality, but also with a higher risk of subsequent cardiac events and higher cost. Efforts to identify a specific cutoff value below which the prognosis is not impaired have not been successful. Rather, the risk of adverse outcomes increases with any elevation of CK or CK-MB and increases further in proportion to the level of intervention. This information complements similar previous data on CABG. Obtaining preprocedural and postprocedural ECGs and measurement of serial cardiac enzymes after revascularization are recommended. Patients with enzyme levels elevated more than threefold above the upper limit of normal or with ECG changes diagnostic for Q wave myocardial infarction (MI) should be treated as patients with an MI. Patients with more modest elevations should be observed carefully. Clinical trials should ensure systematic evaluation for myocardial necrosis, with attention paid to multivariable analysis of risk factors for poor long-term outcome, to determine the extent to which enzyme elevation is an independent risk factor after considering clinical history, coronary anatomy, left ventricular function and clinical evidence of ischemia. In addition, tracking of enzyme levels in clinical trials is needed to determine whether interventions that reduce periprocedural enzyme elevation also improve mortality.

Angioplasty, Balloon, Coronary↗
PubMed1998

Are interatrial band myocytes maximally hypertrophied in normal canine hearts?

In canine right atrial hypertrophy, the cross-sectional area (Axs) of right atrial myocytes increases, whereas the Axs of the broader interatrial band myocytes does not. In the current study, myocyte reconstructions showed that right atrial myocyte length increased in proportion to Axs in right atrial hypertrophy. On the other hand, mean interatrial band myocyte length in both normal and right atrial hypertrophy dogs was roughly inversely proportional to mean Axs, as expected if interatrial band myocyte volume was constant. Plotting mean Axs vs. myocyte length for individual interatrial band myocytes revealed a distribution whose border defined a maximal volume curve; many myocytes were well beneath that curve. Mononuclear myocytes (generally diploid) were limited by a 65,000-micrometer 3 curve, which many binuclear myocytes (generally tetraploid) surpassed; myocyte ploidy thus constrained myocyte volume. However, because many mononuclear and binuclear myocytes had lower volumes, their failure to hypertrophy cannot be attributed to attainment of the maximal volume possible for their ploidy.

Animals↗
PubMed1995

Regional vascular reserve in canine atria and ventricles during rest and exercise.

Vascular reserve, which defines the capacity for further vasodilation in a given physiological or pathological condition, has not been measured in the canine atria. This study defines, in normal dogs, the regional vascular reserve simultaneously measured in the atria (appendage, nonappendage regions) and in the ventricles during rest and two levels of exercise. Blood flow was determined using 11.4 +/- 0.1 microns radiolabeled microspheres. Vascular reserve (percent for each region) is the ratio of vascular conductance during each condition to maximum vascular conductance. Maximum vascular conductance was estimated by infusing adenosine intravenously. For a given physiological condition regional vascular conductance varied two- to threefold. The vascular reserve of each of the regions decreased progressively from rest to mild exercise to moderate exercise. Regional vascular reserve for both atria, the right ventricle, and the epicardial layer of the left ventricle was essentially uniform for a given condition: rest 93 +/- 0.4%, mild exercise 81 +/- 1.2%, and moderate exercise 69 +/- 1.5%. This similarity in vascular reserve implies that for a given physiological condition a common mechanism precisely regulates myocardial perfusion in these cardiac regions as a function of the total vasodilator capacity.

Adenosine↗
PubMed1994

Regional changes in myocyte structure in model of canine right atrial hypertrophy.

To investigate regional variation of myocyte response to atrial hypertrophy, control dogs were compared with dogs with right atrial hypertrophy created by induction of tricuspid regurgitation; after 1 yr, right atrial-to-body weight ratio increased 122% over controls. One section from the interatrial band, appendage and nonappendage roofs, and nonappendage side of each atrium of each dog was stained to reveal myocyte outlines and transverse tubules; myocyte cross-sectional areas were measured and transverse tubule prevalence was estimated. In control dogs, interatrial band myocytes were significantly larger and had more transverse tubules than other atrial myocytes. With atrial hypertrophy, right interatrial band myocytes did not increase significantly in size, whereas other right atrial myocytes nearly doubled in size, approaching the size of interatrial band myocytes without approaching the content of transverse tubules. Left atrial myocytes did not increase in size. Thus hypertrophic response of atrial myocytes to hemodynamic stress depends on the region in which the myocytes are found, and atrial hypertrophy does not demand transverse tubule proliferation.

Animals↗
PubMed1993

Regional blood flow in canine atria during exercise.

Global and regional atrial blood flow was measured with radioisotope-labeled microspheres in eight dogs during rest and two levels of exercise. Both mean right and left atrial blood flow increased significantly (P < 0.05) to a similar degree with each level of exercise (right atria: 0.27 +/- 0.04, 0.89 +/- 0.11, and 1.57 +/- 0.21 ml.min-1 x g-1; left atria: 0.35 +/- 0.04, 0.90 +/- 0.09, and 1.61 +/- 0.17 ml.min-1 x g-1). Atrial blood flow during exercise is greater than anticipated if increased heart rate was the sole cause. In both right and left atria the ratio of appendage to nonappendage flow was significantly (P < 0.005) less than one during resting conditions (0.42 +/- 0.04 and 0.81 +/- 0.05, respectively), not different from unity during mild exercise, and significantly (P < 0.02) greater than one during moderate exercise (1.10 +/- 0.03 and 1.16 +/- 0.05, respectively). This disparity in the blood flow to the appendage and nonappendage regions suggests that the appendage plays an augmented hemodynamic role during exercise, thus requiring a larger proportion of the nutrient flow.

Animals↗
PubMed1993

Myocardial oxygenation in dogs during partial and complete coronary artery occlusion.

Regional myocardial oxygenation was assessed during partial and complete coronary artery occlusion using near infrared spectroscopy. In eight open-chest dogs, partial occlusions resulting in an approximately 42% decrease in left anterior descending coronary artery (LAD) blood flow produced an approximately 21% decrease in tissue O2 stores (tissue oxyhemoglobin plus oxymyoglobin) and no change in the oxidation level of mitochondrial cytochrome aa3. An approximately 81% reduction in LAD blood flow produced nadir levels of tissue oxyhemoglobin plus oxymyoglobin, maximal levels of deoxyhemoglobin plus deoxymyoglobin, a decline in tissue blood volume, and an approximately 39% decrease in cytochrome aa3 oxidation level. These changes were associated with an approximately 52% decrease from the preischemic baseline in mean transmural myocardial blood flow, measured by radiolabeled microspheres, and an approximately 41% decrease in myocardial O2 consumption. Complete occlusion resulted in further decreases in myocardial blood flow, O2 consumption, tissue blood volume, and cytochrome aa3 oxidation state but also produced increases in tissue O2 stores to above the nadir levels noted during partial occlusion. These results indicate that decreases in O2 delivery during partial coronary occlusion increase O2 extraction to sustain mitochondrial O2 availability, but as little as a 52% reduction in myocardial blood flow produces maximal O2 extraction and depletion of tissue O2 stores. Mitochondrial O2 availability is restricted further during complete occlusion because of limited O2 delivery and, possibly, decreases in tissue blood volume and O2 extraction.

Animals↗
PubMed1992

Early and late outcome following deployment of a new flexible tantalum intracoronary stent in dogs.

A new radiopaque, highly flexible balloon-expandable tantalum stent was tested. Thirty-six of 40 stents were successfully deployed percutaneously in the coronary arteries of 31 dogs. The dogs were given aspirin before, intravenous heparin during, and aspirin alone after the procedure. One dog died at 24 hours because of coronary occlusion following traumatic implantation. Four dogs were put to death early, revealing re-endothelialization by 9 days. Eleven dogs were put to death from 2 weeks to 9 months during long-term follow-up, showing all vessels widely patent with the stent uniformly embedded within a stable neointimal layer. Follow-up arteriography showed patency in all remaining stents up to 1 year, with no perforation or aneurysm formation. Four stents were placed into canine peripheral arteries and were removed percutaneously after deployment. Pathology revealed no significant trauma to involved vessels. This tantalum stent exhibits feasibility of percutaneous deployment, early neointimal formation, low thrombogenicity on long-term aspirin therapy alone, and patency up to 1 year in this canine model.

Animals↗
PubMed1992

Prospective analysis of possible myocardial damage or hemolysis occurring as a result of prolonged autoperfusion angioplasty in humans.

OBJECTIVES: The purpose of this study was to further explore the procedural safety of prolonged (15-min) dilation using an autoperfusion coronary angioplasty balloon by assessing the degree of myocardial damage or hemolysis, if any, occurring as a result of the procedure. BACKGROUND: Prolonged balloon inflation periods may be beneficial during percutaneous transluminal coronary angioplasty. The duration of standard balloon angioplasty is often limited by the occurrence of myocardial ischemia due to loss of anterograde blood flow. Autoperfusion angioplasty allows continued myocardial perfusion during balloon inflation and has previously been shown to reduce but not totally eliminate acute myocardial ischemia during prolonged (up to 15 min) balloon inflation. The risk of intravascular hemolysis as a result of autoperfusion angioplasty has not yet been fully delineated. METHODS: Sixty-two consecutive patients (76% men; mean age 58 years) undergoing elective percutaneous transluminal coronary angioplasty of a single lesion were studied. Serial electrocardiographic and creatine kinase MB isoenzyme data were examined to detect evidence of myocardial damage. Tests for hemolysis (plasma free hemoglobin, serum haptoglobin and serum lactate dehydrogenase) were obtained in the 1st 24 consecutive patients. RESULTS: Inflation time was 14 +/- 4 min (mean +/- SD) and the procedure was successful (less than or equal to 50% residual lesion stenosis) in 59 patients (95%). Electrocardiographic evidence of myocardial infarction (greater than 1 mm persistent ST segment depression, greater than 1 mm ST segment elevation or new Q waves) was not observed in any patient. Cardiac enzyme assays were within the normal range in all patients. No evidence of hemolysis was found in the 24 consecutive patients studied. CONCLUSIONS: We conclude that prolonged autoperfusion angioplasty can be performed in patients without clinical evidence of myocardial damage or hemolysis.

Aged↗
PubMed1992

Gene transfer into coronary arteries of intact animals with a percutaneous balloon catheter.

Genetic manipulation of the vasculature may offer insights into the pathogenesis of coronary artery disease and may lead to gene therapy for disorders such as restenosis after percutaneous coronary angioplasty. The goal of this study was to develop a percutaneous method for gene transfer into coronary arteries of intact animals. Liposomes were used to facilitate transfection in coronary arteries with a plasmid containing the cDNA encoding luciferase. This reporter was chosen since it is not expressed in mammalian cells, and it can be quantified using a sensitive assay (light production). Mongrel dogs were catheterized, and DNA was delivered to coronary arteries via a porous perfusion balloon system. Luciferase expression was measured 3-5 days after the procedure, when the dogs were killed. Luciferase activity in control arteries (n = 12) was no higher than average background activity. Eight of 12 transfected arteries exhibited gene expression, averaging 4.3 +/- 2.1 pg luciferase (p less than 0.01, transfected versus control arteries). In addition, the ability to transfect DNA into femoral arteries without a transfection vehicle was tested. Five dogs were subjected to surgical transfection attempts in their femoral arteries with either DNA alone or DNA plus liposomes. Luciferase was expressed in all 10 femoral arteries; those treated with DNA alone expressed 35.6 +/- 8 pg luciferase, and those treated with DNA plus liposomes expressed 42.3 +/- 14 pg luciferase (p = 0.70). These results demonstrate the use of a percutaneous catheter to achieve gene transfer and expression in coronary arteries of intact dogs and suggest that the efficiency of intra-arterial gene transfer may be similar whether or not a transfection vehicle is used.

Animals↗
PubMed1991

Direct in vivo gene transfer into the coronary and peripheral vasculatures of the intact dog.

Gene therapy approaches have been suggested for the treatment of cardiovascular disease. Recently, direct transfer of the gene encoding beta-galactosidase into peripheral arteries of the pig has been demonstrated. To determine whether this approach is applicable to other arterial beds and to other species, we first evaluated the use of beta-galactosidase as a marker protein in the canine model. We demonstrate that variable but substantial endogenous beta-galactosidase-like activity is induced by manipulation of canine peripheral arteries, which precludes the use of this marker protein in evaluating the efficiency of gene transfer in this model. A marker gene encoding firefly luciferase was then evaluated, and background luciferase activity was found to be low in the dog even after arterial manipulation. Using the luciferase gene, we then demonstrated lipid-mediated gene transfer directly into both coronary and peripheral arteries of the intact dog. These results indicate the feasibility of in vivo gene transfer into coronary arteries and demonstrate the use of the luciferase marker protein in quantifying recombinant protein expression following gene transfer in canine models. This simple and effective method for direct in vivo gene transfer into coronary and peripheral arteries may be applicable to the localized production of therapeutically important proteins for the treatment of cardiovascular diseases.

Animals↗
PubMed1990

Dynamic mechanisms of cardiac oxygenation during brief ischemia and reperfusion.

Myocardial oxygenation may be altered markedly by changes in tissue blood flow. During brief ischemia and reperfusion produced by transient occlusion of the left anterior descending artery in 10 open-chest dogs, changes in the oxygenation of tissue hemoglobin (Hb) plus myoglobin (Mb) and the oxidation-reduction (redox) state of mitochondrial cytochrome aa3 were monitored continuously using near-infrared spectroscopy. The nondestructive optical technique indicated that coronary occlusion produced an abrupt drop in tissue oxygen stores (tHb02 + Mb02), tissue blood volume (tBV), and the oxidation level of cytochrome aa3. Changes in the cytochrome oxidation state were related inversely to transmural collateral blood flow within the ischemic region (r = 0.77) measured with radiolabeled microspheres. Furthermore, there was a direct relationship (r = 0.91) between collateral blood flow and the tissue level of desaturated Hb and Mb (tHb + Mb). Reperfusion after 2 min of ischemia led to a synchronous overshoot of baseline in coronary flow and tBV followed by supranormal increases in tHb + Mb02 and the oxidation level of cytochrome aa3. The tHb + Mb level increased transiently during reperfusion. This response correlated inversely with collateral flow during ischemia (r = 0.91). Accordingly, the time required to reach peak tHb + Mb levels was shortest in dogs with high collateral flows (r = 0.75). Thus collateral blood flow partially sustains myocardial oxygenation during coronary artery occlusion and influences tissue reoxygenation early during reperfusion.

Animals↗
PubMed1989

Regional atrial blood flow in dogs. Effect of hypertrophy on coronary flow reserve.

Little is known regarding regional atrial blood flow responses during varying hemodynamic states in both the normal and hypertrophied atria. This study was undertaken to develop a canine model of chronic atrial hypertrophy and to define in both this group and in normal dogs the regional blood flow response to acute atrial fibrillation and to measure coronary flow reserve. In the 12 dogs with atrial but not ventricular hypertrophy the mean left and right atrial weights were 75 and 47% respectively greater than in the normal group. Blood flow in the normal dogs was less in the appendage than in the non-appendage region for both atria and increased significantly during atrial fibrillation. Similar findings were noted in the hypertrophy group except that during control conditions the left atrial appendage flow was similar to the nonappendage flow. Minimal vascular resistance for the hypertrophy group, 39 +/- 3 was significantly (P less than 0.05) greater when compared to the normal group 28 +/- 2 mmHg/cm3 per min per g. Thus, significant regional blood flow differences occur in both the normal and hypertrophied atria. In addition, atrial hypertrophy does not alter the autoregulatory capacity to the hemodynamic stress of atrial fibrillation but does reduce coronary flow reserve.

Animals↗
PubMed1987

Validation of in vivo two-dimensional echocardiographic dimension measurements using myocardial mass estimates in dogs.

The accuracy of in vivo measurements of left ventricular wall thickness and chamber size by means of two-dimensional echocardiography was investigated by comparing left ventricular mass estimates obtained at end diastole in 15 closed-chest dogs with a wide range of left ventricular weights. The systolic and diastolic echocardiographic mass estimates were compared with the actual weights of the freshly excised, stripped left ventricles immediately following death. The mean +/- SD of the weighed mass of the excised ventricles was 104 +/- 25 gm. The mean predicted left ventricular mass with the use of the cylinder-ellipse geometric model and gross anatomic sections corresponding to the echocardiographic imaging planes was 106 +/- 26 gm (r = 0.97 compared to the actual weight). The mean echocardiographic estimate of left ventricular mass at end diastolic was 107 +/- 24 gm (r = 0.98 compared to the weight) and 105 +/- 26 gm at end systole (r = 0.95 compared to the weight). The correlation between the echocardiographic mass estimate at end diastole and the echo mass estimate at end systole was 0.95. Regression analysis failed to demonstrate a significant over- or underestimation of the actual weight by the calculated mass with the use of either the gross anatomic or the in vivo echocardiographic dimension measurements.

Animals↗
PubMed1987

Effect of atrial natriuretic factor on transmural myocardial blood flow distribution in the dog.

These studies were designed to define the effect of atrial natriuretic peptide (ANP) on coronary flow. ANP was infused as a bolus directly into the left circumflex coronary artery in doses ranging from 0.05 to 5 micrograms in nine open-chest, anesthetized dogs. Coronary flow was measured with an electromagnetic flowmeter. Regional transmural myocardial blood flow and distribution were measured with 11.3 +/- 0.25 micron radionuclide-labeled microspheres. No significant change was noted in systemic hemodynamics (heart rate, arterial pressure, left atrial pressure, or cardiac output) during the course of the studies. ANP produced a transient vasodilatation of coronary resistance vessels and increased flow by 41% after both the 2.5 and 5 micrograms doses. The vasodilatation occurred uniformly throughout the ventricular wall so that the endocardial/epicardial flow ratio remained constant. There was no evidence of coronary vasoconstriction. The peak vasodilatation response occurred 28 +/- 7 sec after the beginning of the infusion of ANP and lasted approximately 3 min. These data support the hypothesis that ANP administration is associated with a vasodilator response in the coronary resistance vessels that may be modulated through either the release of another vasodilator substance or another mechanism.

Animals↗