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Biomedical subjects

R M Watson

Publications and source records attributed to R M Watson.

At least 91 records · Page 5Linked to original sources
PubMed1989

Osseointegrated implants--principles and practice: 1. Osseointegration and surgical techniques with the Nobelpharma implant system.

In this series of three articles the authors describe some of the principles and practice of osseointegrated implants. Part 1 gives a detailed description of the surgical techniques required to establish osseointegrated implant fixtures (with special reference to the Branemark system). The article then gives guidance on patient selection and treatment planning. Part 2 will go on to consider prosthetic rehabilitation using osseointegrated implant fixtures. Part 3 will conclude the series by presenting a number of case studies.

Alveolar Process↗
PubMed1989

Osseointegrated implants--principles and practice: 3. Case treatments with the Nobelpharma implant system.

In this series of three articles the authors describe some of the principles and practice of osseointegrated implants. Part 1 gave a detailed description of the surgical techniques to establish osseointegrated implants (with special reference to the Branemark system), guidance on patient selection and treatment planning. Part 2 described prosthetic rehabilitation using osseointegrated implant fixtures. This article concludes the series by presenting a number of case studies.

Adult↗
PubMed1989

Osseointegrated implants--principles and practice: 2. Prosthetic rehabilitation with osseointegrated implants.

In this series of three articles the authors describe some of the principles and practice of osseointegrated implants. Part 1 gave a detailed description of the surgical techniques required to establish osseointegrated implant fixtures (with special reference to the Branemark system), and gave guidance on patient selection and treatment planning. Part 2 now considers prosthetic rehabilitation techniques with osseointegrated implants for complete dentures, complete overdentures, partial bridges, and single tooth replacement cases. Part 3 will conclude the series by presenting a number of case studies.

Dental Implantation, Endosseous↗
PubMed1988

Relation between serum nifedipine concentration and hemodynamic effects in nonobstructive hypertrophic cardiomyopathy.

The relation between nifedipine concentration and hemodynamic effects after sublingual administration of 10 or 20 mg was examined in 13 patients with nonobstructive hypertrophic cardiomyopathy (HC). Serum nifedipine concentrations were determined by gas chromatography and were not related to dose. Peripheral vascular resistance decreased as a function of nifedipine concentration (r = -0.63, p less than 0.001); this was associated with a concentration-related increase in heart rate (r = 0.56, p less than 0.001) and in cardiac index (r = 0.50, p less than 0.001). However, evidence for a pure vasodilator effect of nifedipine was inconsistent, in that the change in stroke volume index with nifedipine was not significant. Although stroke volume index increased at nifedipine concentrations between 60 and 120 ng/ml (38 +/- 6 to 42 +/- 4 ml/m2, p less than 0.01), it decreased at concentrations greater than 120 ng/ml (40 +/- 3 to 38 +/- 4 ml/m2, p less than 0.01). Moreover, pulmonary artery wedge pressure increased at nifedipine concentrations greater than 120 ng/ml (11 +/- 2 to 16 +/- 4 mm Hg, p less than 0.001), suggesting either depressed left ventricular (LV) systolic function or reduced LV filling. To investigate these possible mechanisms, LV systolic and diastolic function was studied during catheterization with a nonimaging scintillation probe in 6 of the 13 patients. In these subjects, heart rate was held constant by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Cinevideodensitometric analysis of the effect of coronary angioplasty on coronary stenotic dimensions.

The accuracy and reproducibility of caliper and cinevideodensitometric measurements of coronary stenotic dimensions were compared in radiographic phantom models and in coronary arteriograms of 28 patients undergoing coronary angioplasty. Projected, single-plane coronary cine frames were analyzed by a computer-assisted videodensitometric method, which measures stenotic cross-sectional area without assumptions about lesion geometry. The accuracy (2.4%) and precision (+/- 1.9%) of cinevideodensitometry for measuring percent area stenosis in Plexiglas models of eccentric stenotic lesions was superior to the accuracy (24.7%) and precision (+/- 5.4%) of caliper measurements. Interobserver variability was significantly (p less than 0.05) better for cinevideodensitometric (r = 0.98; SEE = 6.4%) than for caliper measurements (r = 0.87; SEE = 13.1%). After angioplasty, percent diameter stenosis measured by calipers fell from 70 +/- 12% to 30 +/- 15%. Mean percent area reduction measured by cinevideodensitometry fell from 89.1 +/- 8% to 40.1 +/- 22% and stenotic area increased five-fold, from 0.59 +/- 0.5 to 3.47 +/- 1.6 mm2. Pre and post PTCA gradients did not correlate with lesion dimensions. Cinevideodensitometric measurements of absolute stenotic dimensions were more reproducible than relative measurements expressed as a percentage, due to the tapered caliber of normal arterial segments. Thus, cinevideodensitometric measurements were more accurate and reproducible than caliper measurements. The angiographic effects of coronary angioplasty are best measured by cinevideodensitometry, because residual lesions post PTCA are often eccentric, have indistinct margins, and are better characterized by changes in area than by changes in diameter.

Angioplasty, Balloon↗
PubMed1987

Relation between extent of left ventricular hypertrophy and occurrence of ventricular tachycardia in hypertrophic cardiomyopathy.

This study was undertaken to determine whether the occurrence of ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HC) is related to the magnitude and extent of left ventricular (LV) hypertrophy. Extent of LV hypertrophy was assessed using 2-dimensional echocardiography in 30 patients with HC in whom VT had been documented on 24-hour ambulatory electrocardiographic (ECG) monitoring, and the extent of LV hypertrophy in these patients was compared with that of a control group of 61 patients with HC who had normal ambulatory ECG recordings. Severe LV hypertrophy, involving at least 3 of the 4 LV segments, occurred significantly more often in patients with documented VT (16 of 30, 53%) than in those with normal ambulatory ECG findings (13 of 61, 21%; p less than 0.002). Conversely, mild LV hypertrophy, involving only 1 LV segment, occurred significantly less often in patients with VT (5 of 30, 17%) than in the control subjects (32 of 61, 52%; p less than 0.001). Moderate LV hypertrophy, involving 2 of the 4 LV segments, occurred about as frequently in patients with VT (9 of 30, 30%) as in patients with normal ambulatory ECG findings (16 of 61, 26%; p greater than 0.05). In addition, the LV wall thickness index, a quantitative measure of overall extent of LV hypertrophy, was also significantly higher (thereby indicating a greater magnitude of hypertrophy) in patients with documented VT (72 +/- 17 mm) than in those with normal ambulatory ECG recordings (61 +/- 14 mm; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Three year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty.

Because the long-term anatomic effects of percutaneous transluminal coronary angioplasty are unknown, follow-up evaluations including coronary angiography, treadmill exercise testing and rest and bicycle exercise radionuclide angiography were performed in 46 patients 6.3 +/- 2.0 and 37.6 +/- 3.6 (mean +/- SD) months after they had undergone successful single lesion angioplasty. The severity of the coronary stenosis decreased significantly at each evaluation; the mean diameter stenosis was 66 +/- 13% before angioplasty, 30 +/- 13% immediately after and 26 +/- 16% and 19 +/- 13% at 6 months and 3 years, respectively. Exercise time increased from 9.8 +/- 4.4 minutes before angioplasty to 18.3 +/- 4.5 minutes immediately after the procedure and remained at that level at 6 months (20.3 +/- 4.6 minutes) and 3 years (18.2 +/- 4.5 minutes). Left ventricular ejection fraction during exercise decreased 4 +/- 6% compared with rest before angioplasty, but increased 7 +/- 7% immediately after angioplasty and this increase was maintained at 6 months (+/- 6 +/- 7%) and 3 years (+/- 4 +/- 6%). Before angioplasty, 1 patient was in Canadian Heart Association functional class 0, 15 were in class II, 24 in class III and 6 in class IV. Three years later, 25 were in class 0, 10 in class I, 7 in class II and 4 in class III. These results indicate that the short-term anatomic and functional success of coronary angioplasty is maintained for at least 3 years.

Adult↗
PubMed1987

Inducible polymorphic ventricular tachycardia and ventricular fibrillation in a subgroup of patients with hypertrophic cardiomyopathy at high risk for sudden death.

This investigation was undertaken to elucidate the underlying electrophysiologic substrate in hypertrophic cardiomyopathy and to identify possible predictors of sudden death in this patient population. Programmed stimulation was performed in 18 patients aged 14 to 64 years (mean 36) believed to be at high risk for sudden death on the basis of prior cardiac arrest or syncope, nonsustained ventricular tachycardia on Holter ambulatory electrocardiographic (ECG) monitoring or a family history of frequent sudden death. Polymorphic ventricular tachycardia that deteriorated to ventricular fibrillation was reproducibly induced in 8 (44%) of the 18 patients (Group A). This rhythm was induced in all three patients with a history of cardiac arrest. No sustained monomorphic ventricular tachycardia was induced. Group B comprised the 10 patients in whom a sustained arrhythmia could not be reproducibly initiated. The electrophysiologic substrate was distinctly different in patients with, than in those without, inducible sustained arrhythmia. The refractory period was shorter at the right ventricular outflow tract (232 +/- 22 ms) compared with the apex (264 +/- 12 ms) in Group A (p less than 0.005) whereas there was no difference in Group B (271 +/- 25 ms versus 271 +/- 13 ms). The local ventricular electrogram of most patients in both groups was prolonged and markedly multiphasic. However, 5 of the 8 Group A patients exhibited a double electrogram (V-V') with premature stimulation compared with 1 of the 10 patients in Group B (p less than 0.02). A positive R wave in lead aVR of the scalar ECG and poor R wave progression in the precordial leads were more common in Group A than in Group B (p less than 0.001 and p less than 0.001, respectively). The reason for the distinctly different electrophysiologic substrate and the high prevalence of inducible polymorphic arrhythmia is unclear. It may relate to the underlying myocardial architecture in these patients, characterized by myocardial cellular disarray and fibrosis.

Adolescent↗
PubMed1986

Respiratory function in aboriginal children.

One hundred and fifty-one Aboriginal school children and 246 non-Aboriginal children, all aged between 11 and 15 years, performed lung function tests with a Vitalograph spirometer. The results showed that the mean forced vital capacity was 20% larger in non-Aboriginal children of both sexes. Similar differences were found for the one-second forced expiratory volume, which was 15% larger for the non-Aboriginal boys and 17% larger for the non-Aboriginal girls. Comment is made on their smoking practices.

Adolescent↗
PubMed1986

Conjunctival oxygen tension and its relationship to arterial oxygen tension.

Using a miniaturized Clark electrode embedded in a polymethylmethacrylate eyepiece, we measured transconjunctival oxygen tension (PcjO2) in 5 healthy volunteer subjects at multiple levels of steady-state isocapnic hypoxia, normoxia, and hyperoxia. PcjO2 was linearly related to arterial oxygen tension (PaO2) as PaO2 ranged from 28 to 205 mm Hg (PcjO2 = 0.59 PaO2 + 0.36 mm Hg; r = 0.94; standard error of the estimate = 7.09 mm Hg). However, the relationships between PcjO2 and PaO2 varied significantly among subjects. Whereas the overall mean ratio of PcjO2 to PaO2 was 0.59, the mean ratio for subjects ranged from 0.47 to 0.79 and was significantly different among subjects (P less than 0.0001). The time response of the electrode to a step change in oxygen tension in vitro was exponential, with a 90% response time of 38 seconds after a lag of 3.7 seconds. The time responses to in vivo changes in oxygen tension were also exponential. From hypoxia to normoxia, 90% response time was 45.0 seconds after a lag of 5.1 seconds; from room air to hypoxia, 90% response time was 72.4 seconds after a lag of 30.3 seconds; from room air to hyperoxia, 90% response time was 87.2 seconds after a lag of 6.8 seconds. We conclude that, although PcjO2 measured by a miniaturized Clark electrode is linearly related to PaO2 in healthy subjects, variation in the relationship of PcjO2 to PaO2 among individuals will prevent precise estimation of PaO2 for any individual unless subject-specific calibration is performed.

Adult↗
PubMed1986

Range of accuracy of two wavelength oximetry.

Earlier reports of a two wavelength oximeter suggested a tendency toward overestimation of arterial oxygen saturation (SaO2) at the lowest values examined. To investigate this possible inaccuracy, we compared oximeter readings to SaO2 over a wider range of laboratory-induced steady-state hypoxia than has previously been reported. For values of SaO2 greater than 75 percent, oximeter readings were linearly related to SaO2 such that y = 0.94 SaO2 + 8.7 (r = 0.96) and the mean difference between oximeter reading and SaO2 was 0.09 percent. However, when SaO2 was less than 75 percent, the instrument readings were progressively higher than the SaO2 so that when SaO2 was approximately 50 percent, the oximeter reading was approximately 65 percent. These data show that the two wavelength oximeter displays falsely elevated readings when the arterial saturation falls below 75 percent.

Adult↗
PubMed1986

Fetal wastage in women with anti-Ro(SSA) antibody.

Retrospective obstetric histories were obtained in 50 anti-Ro(SSA) antibody positive women (aged 15-50 years) and 47 anti-nRNP antibody positive women of similar age range. Twenty (40%) anti-Ro(SSA) positive women and 33 (70%) anti-nRNP positive women fulfilled the revised ARA criteria for systemic lupus erythematosus (SLE). Thirty-four anti-Ro(SSA) positive women had a total of 84 pregnancies with a fetal loss of 28%; 29 anti-nRNP positive women had a total of 63 pregnancies with a fetal loss of 19%. Although the overall frequency of fetal wastage between the 2 groups was not significantly different, analysis of the subgroup of SLE patients demonstrated a significantly greater fetal wastage in black anti-Ro(SSA) positive women (15 of 21, 71%) compared with black anti-nRNP positive women (5 of 28, 18% p less than .001). No significant difference in fetal wastage was noted between either the white SLE or the non-SLE women in either antibody group. These data suggest that black SLE patients with anti-Ro(SSA) antibody may be at increased risk of fetal wastage.

Abortion, Spontaneous↗
PubMed1985

Efficacy of calcium channel blocker therapy for angina pectoris resulting from small-vessel coronary artery disease and abnormal vasodilator reserve.

Abnormal vasodilator reserve of the coronary microcirculation is a frequent mechanism of angina pectoris in patients with angiographically normal coronary arteries. To assess the effect of calcium channel blocking agents on symptoms and exercise capacity, 26 patients shown to have angina pectoris because of abnormally small coronary arteries and limited vasodilator reserve underwent randomized, double-blind, placebo-controlled outpatient study, with 1 month for each period. An unblinded lead-in phase determined the best dose of verapamil (17 patients) or nifedipine (9 patients). Exercise testing using bicycle ergometry was performed at the end of each period. Four patients interrupted the placebo period and 1 patient interrupted both placebo and drug period because of frequent and severe chest pain. While receiving calcium channel blocker drugs, patients who completed both phases of the study recorded fewer episodes of angina (21 +/- 21 vs 35 +/- 27, p less than 0.001) and consumed fewer nitroglycerin tablets (23 +/- 27 vs 41 +/- 50, p less than 0.001) than during the placebo period. Exercise duration was slightly but significantly prolonged (278 +/- 129 vs 231 +/- 136 seconds, p less than 0.025) during drug treatment compared with placebo, and significantly fewer patients terminated exercise with chest pain while receiving drug treatment. Subjectively, 22 of 26 patients felt better on the calcium channel blocker than on placebo. Thus, calcium channel blocker therapy appears to be beneficial in controlling angina and improving exercise tolerance in patients with angina pectoris resulting from abnormally small coronary arteries and limited vasodilator reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Chest pain and "normal" coronary arteries--role of small coronary arteries.

To study the mechanism of chest pain in patients with insignificant epicardial coronary artery disease, 50 patients underwent great cardiac vein (GCV) flow, oxygen content and lactate determinations at rest and during pacing, and left ventricular end-diastolic pressure (LVEDP) measurements at rest and after pacing. Twenty-four patients having typical chest discomfort during pacing demonstrated significantly lower increase in flow from baseline (36 +/- 18% versus 86 +/- 24%, p less than 0.001) and decrease in coronary resistance (-17 +/- 12% versus -43 +/- 7%, p less than 0.001) compared with 26 patients without pacing-induced chest pain, despite no significant difference in myocardial oxygen consumption (MVO2) between the 2 groups. Lactate consumption at a heart rate (HR) of 150 beats/min was significantly less (28.3 +/- 21.5 versus 51.3 +/- 35.8 mM X ml/min, p less than 0.001) and the increase in LVEDP from rest to after pacing was significantly greater (5 +/- 2 versus 1 +/- 2 mm Hg, p less than 0.001) in the chest pain group. After administration of ergonovine, 0.15 mg intravenously, to 46 of these patients, 31 had typical pain either at rest (1 patient) or during pacing. This group had significantly lower increase in flow (38 +/- 20% versus 107 +/- 38%, p less than 0.001), and decrease in coronary resistance (-16 +/- 12% versus -45 +/- 11%, p less than 0.001) compared with the 15 patients not having chest pain, despite no significant difference in MVO2 between the 2 groups. Patients with chest pain also had lower lactate consumption at a HR of 150 beats/min (39.2 +/- 23.6 versus 65.3 +/- 46.3 mM X ml/min, p less than 0.01), greater arterial-GCV oxygen difference (12.5 +/- 1.3 versus 11.6 +/- 1.0 ml O2/100 ml, p less than 0.05), and a more marked increase in LVEDP from rest to after pacing (11 +/- 3 versus 5 +/- 2 mm Hg, p less than 0.001). Quantitative coronary arteriography demonstrated no significant luminal narrowing of the epicardial coronary arteries in response to ergonovine. These data are consistent with the hypothesis that some patients with chest pain and angiographically normal epicardial coronary arteries have dynamic abnormalities of the small coronary arteries or coronary microcirculation that cause abnormal vasodilator reserve or vasoconstriction, resulting in myocardial ischemia and angina pectoris.

Adult↗
PubMed1985

Dynamic coronary obstruction as a cause of angina pectoris: implications regarding therapy.

The strong link demonstrated at autopsy between coronary atherosclerosis and angina pectoris led to the important concept that a fixed obstruction of 1 or more coronary arteries was the pathophysiologic cause of angina: myocardial ischemia and angina occurred when myocardial oxygen demand out-stripped the capacity of the diseased coronary artery to deliver oxygen. Therapeutic strategies were based on attempts to lower myocardial oxygen needs induced by physical and emotional stress. However, the finding that dynamic increases in coronary vascular resistance can also either precipitate ischemia or reduce the threshold of myocardial oxygen consumption (MVO2) at which it occurs has profoundly altered our understanding of the pathophysiologic features of angina and, therefore, its treatment. Dynamic coronary obstruction can occur at the large-vessel level, causing Prinzmetal's or variant angina. It is also possible that in some patients a continuum of large-vessel coronary vasoconstrictor tone exists, causing the common clinical situation manifested by angina with variable thresholds of onset. Recent studies have demonstrated that increases in the resistance offered to flow by small coronary arteries too small to be imaged by angiography can also decrease anginal threshold. The fact that ischemia can be precipitated by dynamic increases in large- or small-vessel coronary resistance has important implications for the therapy of angina pectoris. In those persons who mostly have a dynamic component contributing to their coronary obstruction, primary intervention with vasodilator therapy, including nitrates and calcium-channel blocking agents, are probably most effective therapeutically.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗