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Biomedical subjects

T J Ryan

Publications and source records attributed to T J Ryan.

At least 19 recordsLinked to original sources
PubMed1992

Prediction of risk for hemodynamic compromise during percutaneous transluminal coronary angioplasty.

The availability of circulatory support devices has increased the importance of accurately identifying patients at risk for hemodynamic compromise during percutaneous transluminal coronary angioplasty (PTCA). Accordingly, prospective evaluation of 3 criteria to predict hemodynamic compromise (defined as a decrease in systolic blood pressure > or = 20 to < 90 mm Hg during balloon inflation) in 157 patients (group A) undergoing PTCA was performed. Left ventricular ejection fraction < 35% had a sensitivity of 13% and a specificity of 95%. Greater than 50% of the myocardium at risk was associated with a sensitivity of 31% and a specificity of 85%. The angiographer's assessment of high risk for hemodynamic compromise had the highest sensitivity of 56% and a specificity of 86%. The clinical and angiographic characteristics of these patients were reviewed to identify risk factors retrospectively. Multivariate analysis of 28 variables identified multivessel disease, diffuse disease, myocardium at risk, and stenosis before PTCA as independent predictors of hemodynamic compromise. With use of this analysis, a 13-point weighted scoring system was created based on the regression of coefficients of the variables. Defining high risk for hemodynamic compromise as a risk score > or = 4, the sensitivity of this criterion in group A patients was 81% and the specificity was 74%. The scoring system was then prospectively applied to 61 consecutive patients (group B) undergoing PTCA. In using a risk score > or = 4 to define high risk, this scoring system had a sensitivity of 92% and a specificity of 92%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Safety and clinical use of exercise testing one to three days after percutaneous transluminal coronary angioplasty.

To evaluate both the safety and clinical use of predischarge symptom-limited exercise testing after successful uncomplicated percutaneous transluminal coronary angioplasty (PTCA), 100 patients were randomized to undergo exercise testing (n = 50) or no exercise testing (n = 50). There were no differences in clinical or angiographic characteristics between the groups. Exercise testing was performed 38 +/- 14 hours after PTCA. Patients who exercised achieved 71 +/- 12% of predicted maximal heart rate, with 38% reaching greater than or equal to stage III of the Bruce protocol. No patient in either group developed cardiac complications during 48-hour follow-up. Of the 11 patients with a positive test result, 92% had angiographically incomplete revascularization. Attending physicians (n = 16) were questioned both before and after exercise testing about when, after discharge, they would allow their patient to perform each of 11 specific activities of daily living. Questionnaires were administered to physicians at similar time frames for patients in the no-exercise group. Comparison of the responses between initial and repeat questionnaires showed that patients in the exercise group (with a test result negative for ischemia) were allowed to perform 7 of 11 activities, including return to work, earlier (p less than 0.05) than the no-exercise patients. These data indicate that in this well-defined group of patients, symptom-limited exercise testing early after PTCA appears to be safe, and alters physician management in allowing patients with a negative test result to return to various activities at an earlier date. Such testing may be useful in counseling patients after PTCA.

Activities of Daily Living↗
PubMed1992

Comparison of the clinical profile and outcome of women and men in cardiac rehabilitation.

Few data are available regarding the outcome of women in cardiac rehabilitation. To determine whether women differ from men in clinical profile and outcome, 225 consecutive patients were prospectively evaluated in an urban, multidisciplinary, exercise-based cardiac rehabilitation program. Among the 51 women (age 56 +/- 10) and 174 men (age 54 +/- 10), most were: white (84%), married (64%), employed (63%), had had myocardial infarction or revascularization, or both (66%), and traveled less than 10 miles to the program (92%). Risk profiles revealed obesity in 48% (mean Metropolitan Relative Weight = 124 +/- 22%), hypertension in 47%, smoking in 23%, diabetes in 16%, and mean cholesterol of 236 +/- 45 mg/dl. Compared with men, more women were nonwhite, unemployed, unmarried, hypertensive or diabetic (p less than 0.0001) and had higher cholesterol (p less than 0.01). Compliance rates were similar for women (51%) and men (63%) (p = not significant). Univariate predictors of program noncompliance differed between women and men. Initial exercise capacity was less for women than for men, but both groups achieved a similar training effect. Women increased their exercise time by 31% and peak METs by 30%, whereas men showed a 21% increase in exercise time and 16% increase in peak METs achieved (p less than 0.001). Thus, in this cardiac rehabilitation program, women have a less favorable risk factor profile and differ from men with regard to baseline demographics and predictors of program completion. Women, however, have similar rates of compliance and achieve the same improvement in functional capacity with training.

Adult↗
PubMed1992

Abnormal endothelium-dependent coronary vasomotion in hypertensive patients.

Coronary vasomotion is abnormal in hypertensive patients, as evidenced by reduced coronary vasodilator reserve, but endothelium-dependent coronary vasomotion in hypertensive patients has not been studied. To assess the integrity of endothelium-dependent vasodilation, the response of coronary arteries to acetylcholine (an endothelium-dependent vasodilator) and nitroglycerin (an endothelium-independent vasodilator) was studied in 14 patients undergoing cardiac catheterization. Eight patients with essential hypertension were compared with six normotensive patients. None had obstructive disease detectable by coronary arteriography. Coronary artery diameter was measured with digital-subtracted arteriography and coronary blood flow velocity with a Doppler flow velocity catheter. At baseline, coronary artery diameter was similar in the hypertensive and the normotensive control patients (2.4 +/- 0.3 vs. 2.8 +/- 0.7 mm). During intracoronary acetylcholine infusion (30 micrograms/min), coronary artery diameter decreased to 1.3 +/- 0.7 mm in the hypertensive patients (p less than 0.005), but was unchanged (2.7 +/- 0.8 mm) in the normotensive patients. With intracoronary nitroglycerin (200 micrograms), coronary artery diameter increased significantly in both groups. Calculated coronary blood flow decreased during acetylcholine infusion by 59 +/- 31% in the hypertensive patients but increased by 3 +/- 3% in the normotensive group (p less than 0.005). There was a significant negative correlation between the percent change in estimated coronary blood flow during acetylcholine infusion and mean arterial pressure measured at baseline (r = 0.67, p less than 0.02). Therefore, these hypertensive patients exhibited marked coronary vasoconstriction in response to intracoronary acetylcholine but normal vasodilation in response to nitroglycerin, suggesting abnormal endothelium-dependent vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Comparison of ischemic and physiologic responses during exercise tests in men using the standard and modified Bruce protocols.

The importance of low-level (warm-up) exercise for reducing exercise-induced myocardial ischemic symptoms in patients with coronary artery disease is well-recognized by clinicians. Whether altering the abruptness of exercise, such as that which occurs during different frequently used testing protocols, affects myocardial ischemic variables and maximal exercise capacity has not been resolved. This study seeks to determine the effects of altering the increment of work-rate change per exercise stage on both the ischemic threshold and maximal exercise capacity using 2 frequently used exercise testing protocols. Thirty-two patients with documented coronary artery disease and previously positive exercise tests (ischemic ST depression greater than or equal to 1.0 mm) performed symptom-limited exercise tests using both the standard and modified Bruce protocols in random order, 1 hour apart. Exercise electrocardiograms were analyzed to determine the ischemic threshold, defined as heart rate at onset of greater than or equal to 1.0 mm ischemic ST depression. Patients achieved a higher peak heart rate (124 +/- 19 vs 117 +/- 21 beats/min; p less than 0.0001), rate-pressure product (21.4 +/- 3.9 vs 19.8 +/- 4.1 beats/min x mm Hg x 10(3); p less than or equal to 0.0001) and oxygen consumption (VO2) (18.5 +/- 3.7 vs 16.5 +/- 4.4 ml/kg/min; p less than or equal to 0.001) with the standard than with the modified Bruce protocol. At matched submaximal exercise stages there were no differences in VO2, heart rate or oxygen pulse between protocols. Time to ischemic threshold was significantly reduced with the standard compared with the modified Bruce protocol (312 +/- 107 vs 607 +/- 221 seconds; p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Plasmin generation induces neutrophil aggregation: dependence on the catalytic and lysine binding sites.

We established that plasmin (10(-10) M to 10(-6) M) caused neutrophils (PMN) to aggregate using an in vitro assay. Plasminogen had no PMN aggregatory activity even at a concentration of 2 microM. However, plasminogen caused PMN to aggregate when incubated with plasminogen activators [tissue plasminogen activator (25-200 U/ml) or urokinase (5-500 U/ml)]. Tissue plasminogen activator and urokinase alone had no PMN aggregatory activity. Analysis of these incubation mixtures indicated that plasmin was generated in the process and that the time course of plasmin generation correlated with the aggregation response. Active-site-inhibited plasmin did not induce PMN aggregation, indicating that a functional catalytic site was required for the response. Pretreatment of PMN with either active-site-inhibited plasmin or tranexamic acid prevented PMN aggregation by plasmin, indicating that both binding of plasmin to the cell surface via the lysine binding sites and catalysis were required for the response. The generation of plasmin during activation of fibrinolysis may play a pro-inflammatory role by mediating aggregation of PMN.

Binding Sites↗
PubMed1992

The degree of revascularization and outcome after multivessel coronary angioplasty.

Incomplete revascularization is a common occurrence following angioplasty (PTCA) in patients with multivessel disease. To determine the short-term and long-term consequences of incomplete revascularization and the influence of the functional nature of the incomplete revascularization, 139 consecutive patients with multivessel disease were analyzed: 72 were completely revascularized and 67 had incomplete revascularization. The former patients had a lower incidence of prior myocardial infarction (MI) and prior bypass surgery (CABG). All patients had at least one lesion successfully dilated. In-hospital complications were insignificantly greater in incompletely revascularized patients compared with completely vascularized patients (mortality 3% versus 1%, MI 11% versus 4%, and emergency surgery 5% versus 0%). After 1 year of follow-up, incompletely revascularized patients had similar outcomes (mortality 6% versus 3%, MI 13% versus 7%, CABG 18% versus 15%, and repeat PTCA 19% versus 31%). The degree of incomplete revascularization was categorized as functionally adequate if all stenoses in bypassable vessels supporting viable myocardium were successfully dilated. Significantly fewer adverse events (death, MI, or CABG) occurred in the functionally adequate group than in the functionally inadequate group (27% versus 6%, p less than 0.04). This study demonstrates that incompletely revascularized patients have a favorable 1-year outcome and that patients with incomplete but functionally adequate revascularization have long-term results comparable with those of patients with complete revascularization. This study emphasizes the need to assess the functional significance of a stenosis when considering incomplete revascularization in a patient with multivessel disease.

Angioplasty, Balloon, Coronary↗
PubMed1992

The effect of antiplatelet therapy on platelet accumulation after experimental angioplasty in the rabbit iliac model.

Antiplatelet therapy is routinely used in balloon angioplasty. Yet recent clinical trials have not shown these agents to reduce the incidence of restenosis. As this might be due to inadequate antiplatelet effect, this study was designed to evaluate the effectiveness of antiplatelet therapy in reducing platelet accumulation immediately after angioplasty. Sixty-six atherosclerotic rabbits underwent angioplasty of a focal (50-99%) iliac stenosis after pretreatment with an antiplatelet drug. The animals were randomly given aspirin (10 mg/kg orally) (n = 10), aspirin (10 mg/kg intravenously) (n = 7), aspirin (10 mg/kg per os) plus dipyridamole (25 mg orally) (n = 8), a thromboxane synthetase inhibitor (GS13080, 1 mg/kg/h intravenously) (n = 9) or heparin (500 U/kg intravenously) (n = 9). Platelet accumulation, determined by 51Cr-labeled platelet counts 30 min after angioplasty disclosed a significant reduction from control (44.1 +/- 51.2 platelets/cm x 10(6)) with intravenous aspirin (3.3 +/- 1.9; p less than 0.007) and the thromboxane synthetase inhibitor CGS13080 (15.1 +/- 16.6, p less than 0.04). Aspirin plus dipyridamole reduced platelet accumulation as well (10.4 +/- 9.8, p = 0.076), while oral aspirin (109.5 +/- 240) and heparin (34.7 +/- 35.5) were ineffective. The results of this study demonstrate that pretreatment with antiplatelet agents can reduce platelet accumulation significantly after experimental angioplasty. However, the wide variability in effectiveness particularly with oral aspirin may have important clinical implications. Further investigation into more effective antiplatelet therapy may help to reduce the incidence of abrupt vessel closure and restenosis.

Angioplasty, Balloon↗
PubMed1992

Incidence and prognostic implications of heart block complicating inferior myocardial infarction treated with thrombolytic therapy: results from TIMI II.

OBJECTIVES: The aim of this study was to determine the incidence and significance of second- or third-degree heart block among patients with inferior myocardial infarction treated with thrombolytic therapy. BACKGROUND: Data from the prethrombolytic era suggest that heart block occurs in approximately 20% of patients with acute inferior myocardial infarction and is associated with a marked increase in mortality. Little is known about the incidence and prognostic implications of heart block among patients receiving thrombolytic therapy. METHODS: We studied 1,786 patients with acute inferior myocardial infarction enrolled in the Thrombolysis in Myocardial Infarction (TIMI) II Trial who received recombinant tissue-type plasminogen activator (rt-PA) within 4 h of the onset of symptoms. RESULTS: Heart block occurred in 214 patients (12%); 113 (6.3%) had heart block on presentation and 101 (5.7%) developed heart block in the 24 h after treatment with rt-PA. Patients with heart block at entry were slightly older and a greater proportion had cardiogenic shock. The 21-day mortality rate among patients with heart block at entry was 7.1% (8 of 113), compared with 2.7% (45 of 1,673) among patients without heart block at study entry (relative risk 2.6, p = 0.007). However, heart block was not independently associated with 21-day mortality after adjustment for other variables, including shock. Mortality and other adverse cardiac events in the following year were similar among patients with and without heart block. Among patients without heart block at study entry, coronary angiography among patients randomly assigned to coronary catheterization 18 to 48 h after admission revealed that the infarct-related artery was occluded in 28.2% (11 of 39) of patients who developed heart block versus 15.5% (112 of 723) of patients without heart block (p = 0.04). The 21-day mortality rate was increased among patients in whom heart block developed after thrombolytic therapy (9.9% [10 of 101] versus 2.2% [35 of 1,572] of patients without heart block, relative risk 4.5, p less than 0.001). Analysis of the increased mortality among patients who developed heart block suggests that mortality was due to severe cardiac dysfunction; no patient was considered to have died as a result of the heart block or its treatment. CONCLUSIONS: Heart block is common among patients with inferior infarction given thrombolytic therapy and is associated with increased mortality. These clinical and anatomic data provide insight into the mechanism of heart block and increased mortality among such patients.

Female↗
PubMed1992

Invasive versus conservative strategy after thrombolytic therapy for acute myocardial infarction in patients with antecedent angina. A report from Thrombolysis in Myocardial Infarction Phase II (TIMI II).

OBJECTIVES: This study was designed to assess the possibility that a subgroup of patients at high risk for recurrent ischemia and reinfarction after thrombolytic therapy might benefit from early intervention. BACKGROUND: The Thrombolysis in Myocardial Infarction Phase II (TIMI II) study recently concluded that an obligatory invasive strategy after thrombolytic therapy offered no advantage over a more conservative strategy. METHODS: Data from the 3,534 patients enrolled in the TIMI II trial were analyzed to determine whether a history of antecedent angina before myocardial infarction identifies patients at high risk for subsequent ischemia and whether these patients might benefit from an invasive strategy. RESULTS: Within the TIMI II population, antecedent angina identified patients at increased risk for recurrent chest pain in the hospital (32.3% vs. 22.1%, p < 0.001) and recurrent infarction during the 1st year of follow-up (11.2% vs. 7.9%, p = 0.001) compared with that of patients without antecedent angina. Among patients assigned to the invasive strategy, coronary arteriography revealed that those with antecedent angina had a more severe residual stenosis of the infarct-related artery after thrombolytic therapy (77.1 +/- 0.7% vs. 73.0 +/- 0.9%, p < 0.001) and more multivessel disease (37.9% vs. 26.4%, p < 0.001). The clinical outcome of the patients with antecedent angina assigned randomly to either the invasive or the conservative strategy were compared. The invasive strategy patients had a slightly lesser incidence of recurrent chest pain in the hospital (29.9% vs. 34.8%, p = 0.13) and more negative (normal) findings on exercise tolerance tests (24.7 vs. 18.9%, p = 0.003), but there was no difference between the treatment strategies in the end point variable of recurrent myocardial infarction or death. CONCLUSIONS: These data demonstrate that antecedent angina identifies patients at increased risk for recurrent ischemic events after thrombolytic therapy. However, similar to the results for the overall population, the invasive strategy does not alter the risk of reinfarction or death compared with the conservative approach.

Administration, Oral↗
PubMed1992

Minoxidil-induced changes in the contraction of collagen lattices by human skin fibroblasts.

This investigation has studied the effect of minoxidil on the contraction of hydrated collagen lattices by human dermal fibroblasts. Type I collagen was mixed with a fibroblast suspension and polymerized, and minoxidil 10 to 800 micrograms/ml (0.05 to 4 mM) was added at the time the lattices were released. Minoxidil at concentrations from 100 to 600 micrograms/ml inhibited contraction in a dose-dependent manner, whereas 800 micrograms/ml prevented contraction completely, most cells remaining rounded. Considerable inhibition was already evident within 24 hours. Visualization of living cells with MTT and cell counts showed that inhibition in the first 48 hours was not due to fibroblast death. Exchange of minoxidil to normal medium led to a resumption of contraction and a return to an elongate morphology. Minoxidil at 10 micrograms/ml had no significant effect on lattice contraction, whereas at 100 micrograms/ml it slowed contraction without affecting proliferation or morphology, as observed under the light microscope. The inhibitory effect of minoxidil should be investigated further in relation to the control of contraction of wounds in vivo.

Adolescent↗
PubMed1992

Worldwide strategy for skin health care in a financial strait-jacket.

In consideration of the year 2000, dermatologists must take up the challenge of "Health for All." This paper draws attention to the scope of dermatology, the nature of its work force, the qualifications that are desirable, and the deficiencies and impediments that characterize dermatologic solutions worldwide. It suggests that the future of dermatology depends on achieving appropriate and essential staffing, technology, drugs, and learning materials, within available financial resources. To achieve this, dermatologists must talk more persuasively to those who govern and some centralization of resources into regional training centers may be desirable. Delegation of skin care to purpose-trained auxiliaries, nurses, or medical assistants is essential if costs are to be contained while enlarging the work force.

Delivery of Health Care↗
PubMed1992

Hyperoxia increases plasminogen activator activity of cultured endothelial cells.

Confluent calf pulmonary artery endothelial monolayers exposed to 95% oxygen for 1, 2, or 3 days exhibit a time-dependent increase in adherence to substratum, which closely parallels changes in actin cytoarchitecture and the distribution of focal contact proteins vinculin and talin. Oxygen exposure also resulted in elevated plasminogen activator (PA) activity in conditioned media (CM) and in cytoskeletal protein- and focal contact protein-enriched fractions, with highest levels achieved in the latter two fractions at 48 h after oxygen exposure. PAs have been shown to participate in dismantling of extracellular matrix in a number of physiological and pathological situations. Immunocytochemical studies demonstrated extensive restructuring of matrix proteins collagen IV, laminin, and fibronectin, which correlated temporally with elevated PA levels. Further, when protease-containing cell fractions were used to study degradation of isolated matrices, those obtained from hyperoxia-exposed cells were substantially more active than those from normoxia-exposed cells. Our data suggest that hyperoxia-induced production of PA (and perhaps other proteases) may be partly responsible for degradation of the extracellular matrix of endothelial cells.

Animals↗
PubMed1992

Loss of the coronary microvascular response to acetylcholine in cardiac transplant patients.

BACKGROUND: The coronary arteries of transplanted hearts frequently develop accelerated diffuse arteriosclerosis. The effects of this disease on resistance vessel function are unknown. METHODS AND RESULTS: To investigate the integrity of endothelium-dependent small-vessel vasodilation in transplanted hearts, coronary blood flow (CBF) responses to the endothelium-dependent dilator acetylcholine (10(-8) to 10(-6) M) and the essentially endothelium-independent dilator adenosine (10(-6) to 10(-4) M) were assessed in 40 studies of 29 transplant patients 1-3 years after transplantation and in seven nontransplanted controls. CBF was measured at constant arterial pressure with a Doppler catheter in the left anterior descending coronary artery. Controls, year 1 transplant patients, and year 2 transplant patients had similar increases in CBF in response to acetylcholine (232 +/- 40%, 200 +/- 41%, and 201 +/- 54%, respectively; p = NS), whereas year 3 transplant patients had increased CBF of only 100 +/- 39% (p less than 0.05 versus controls). An index of the proportion of CBF reserve attributable to endothelium-dependent dilation was obtained by normalizing each patient's peak acetylcholine flow response by the peak adenosine flow response. In patients receiving both acetylcholine and adenosine, endothelium-dependent flow responses declined over time [57 +/- 9% in controls, 56 +/- 10% for year 1, 47 +/- 12% for year 2, and 29 +/- 9% for year 3 (p less than 0.05 versus controls)]. An increased mean cyclosporine level (range, 99-261 ng/ml) (r = 0.67, p = 0.004) and increased transplant recipient age (range, 20-63 years) (r = 0.51, p = 0.004) predicted a preserved endothelium-dependent microvascular response. CONCLUSIONS: Thus, microvascular endothelium-dependent dilation deteriorates over time in the transplanted heart, which may reflect underlying graft arteriosclerosis and contribute to ischemic damage of the myocardium.

Acetylcholine↗