PubMed Health⌕ Search

Biomedical subjects

T C Nichols

Publications and source records attributed to T C Nichols.

44 records · Page 3Linked to original sources
PubMed1990

Effect of heparin on coronary arterial patency after thrombolysis with tissue plasminogen activator in acute myocardial infarction.

Infarct artery patency rates at 90 minutes after coronary thrombolysis using recombinant tissue-type plasminogen activator (rt-PA) with and without concurrent heparin anticoagulation have been shown to be comparable. The contribution of heparin to efficacy and safety after thrombolysis with rt-PA is unknown. In this pilot study, 84 patients were treated within 6 hours of onset of acute myocardial infarction (mean of 2.7 hours) with the standard dose of 100 mg of rt-PA over 3 hours. Forty-two patients were randomized to receive additionally immediate intravenous heparin anticoagulation (5,000 U of intravenous bolus followed by 1,000 U/hour titrated to a partial thromboplastin time of 1.5 to 2.0 times control) while 42 patients received rt-PA alone. Coronary angiography performed on day 3 (48 to 72 hours, mean 57) after rt-PA therapy revealed infarct artery patency rates of 71 and 43% in anticoagulated and control patients, respectively (p = 0.015). Recurrent ischemia or infarction, or both, occurred in 3 (7.1%) anticoagulated patients and 5 (11.9%) control patients (difference not significant). Mild, moderate and severe bleeding occurred in 52, 10 and 2% of the group receiving anticoagulation, respectively, and 34, 2 and 0% of patients in the control group, respectively (p = 0.006). These data indicate that after rt-PA therapy of acute myocardial infarction, heparin therapy is associated with substantially higher coronary patency rates 3 days after thrombolysis but is accompanied by an increased incidence of minor bleeding complications.

Coronary Angiography↗
PubMed1990

Coronary artery fistula: an abnormality affecting all age groups.

A coronary artery fistula is an abnormal communication between a coronary artery and a cardiac chamber, great vessel, or other vascular structure. It is an infrequent but potentially important abnormality that can affect any age group. Most are congenital in origin, although other etiologies, in particular trauma, have been identified. Many are small and found incidentally during coronary arteriography, while others are identified as the cause of a continuous murmur, myocardial ischemia, congestive heart failure, or, rarely, bacterial endocarditis. The diagnosis should be considered in any patient presenting with a continuous murmur or in the setting of congestive heart failure, myocardial ischemia, or bacterial endocarditis without an obvious etiology. The pathophysiologic mechanisms resulting in symptoms include cardiac volume overload due to the shunting of blood and reduction of the myocardial blood supply due to "coronary steal." The diagnosis of coronary artery fistula may be suggested by the finding of a continuous murmur in a precordial location, which is atypical for patent ductus arteriosus. Two-dimensional echocardiography may demonstrate dilated coronary arteries, and pulse-wave and color-flow Doppler examinations can display turbulent flow in the suspected fistula and its receiving chamber or vessel. Angiography is generally needed to confirm the diagnosis and elucidate anatomic detail. The natural history of coronary artery fistula is variable, with long periods of stability in some patients and gradual progression of symptoms in others. Small fistulas detected incidentally at the time of angiography do not require immediate surgical correction, but careful follow-up is indicated because the potential for enlargement with physiologically important shunting exists and cannot readily be predicted. Spontaneous closure is uncommon. Surgical repair of the fistula is recommended for symptomatic patients and for some without symptoms because a quantitatively small shunt does not predict freedom from future symptoms or complications. Those selected for medical management must be followed closely.

Adolescent↗
PubMed1989

Limitations of the metabolic rate meter for measuring oxygen consumption and cardiac output.

Over the past few years, a metabolic rate meter has been introduced for easy measurement of oxygen consumption. However, its accuracy is unproved. In 40 patients (26 men, 14 women, ages 34 to 73 years), cardiac output was measured simultaneously by thermodilution and the Fick method using the metabolic rate meter to quantitate oxygen consumption. In comparison with thermodilution, the results using the Fick method were low (5.26 +/- 1.18 vs 4.14 +/- 0.99 liters/min, respectively, p less than 0.01). In 18 patients cardiac output also was measured by the Fick method using a Douglas bag to quantitate oxygen consumption. In these patients, oxygen consumption measured with the metabolic rate meter was lower than that obtained using the Douglas bag (168 +/- 25 vs 216 +/- 42 ml/min, respectively, p less than 0.01). With the Douglas bag, the Fick and thermodilution cardiac output measurements were similar (4.68 +/- 1.08 vs 4.87 +/- 0.86 liters/min, respectively, difference not significant), and they differed by less than or equal to 10% in 15 patients. In contrast, with the metabolic rate meter, the results of thermodilution were higher than those with the Fick method (4.84 +/- 0.95 vs 3.60 +/- 0.71 liters/min, respectively, p less than 0.01), and differed by less than or equal to 10% in only 1 patient (p less than 0.01). Thus, the values for oxygen consumption and cardiac output obtained with the metabolic rate meter are lower than actual values. This device is less accurate than the Douglas bag.

Adult↗
PubMed1989

Nonemergent cardiac catheterization and risk-stratified revascularization following thrombolytic therapy for acute myocardial infarction. A critical analysis of therapy in the community setting. University of North Carolina Cardiology Consortium.

We evaluated a strategy for administering thrombolytic therapy without emergent cardiac catheterization to patients with acute myocardial infarction in community hospitals. Fifty-nine patients were treated with intravenous streptokinase and heparin, and referred for elective catheterization. Angioplasty or bypass surgery was performed only in patients judged to be at risk for reinfarction. One or more predetermined criteria for infarct segment viability were present in 47 (80%) of 59 patients. Angina recurred in 24 patients and enzyme-positive reinfarction in 9 patients, but only 2 patients developed new Q waves or a creatine kinase rise to over twice the normal value. Of 18 patients judged to be at low risk for reinfarction, only 1 required urgent angioplasty or bypass surgery. Fourteen-day mortality was 7% and infarct vessel patency was 94%. These data indicate that physicians in small community hospitals with a close relationship to a referral center and with a carefully designed protocol can administer thrombolytic therapy safely and effectively. By subsequent stratification of patients according to the risk of recurrent infarction, 22% of patients eligible for revascularization were spared urgent angioplasty or bypass surgery.

Angioplasty, Balloon↗
PubMed1987

Prevention of occlusive coronary artery thrombosis by a murine monoclonal antibody to porcine von Willebrand factor.

A murine monoclonal antibody (mAb) against porcine von Willebrand factor (vWF) induced an antithrombotic state in normal pigs. Thrombosis was induced by a standard procedure of stenosis and mechanical injury of the artery. The mAb was an IgG1 kappa that inhibited vWF-induced platelet aggregation at a titer of 1:6250 and bound to immobilized vWF at a maximal dilution of 1:512,000. The antibody did not affect two other vWF functions, platelet adhesion and binding of coagulant factor VIII (factor VIII:C). The antithrombotic state was characterized by a prolonged bleeding time and lack of plasma vWF activity, but with near-normal levels of factor VIII:C and von Willebrand antigen. The circulating Ag.mAb complex demonstrated a multimeric distribution comparable to that of native plasma vWF. Three groups of pigs were studied: group A consisted of nine untreated animals, eight of which developed occlusive coronary thrombosis; group B, four treated animals with a long bleeding time, none of which developed occlusive thrombosis; and group C, two animals with preexisting thrombosis treated with mAb, in which stable blood flow was reestablished. Morphologically, the group B animals showed adherent platelets covering the injured intima but no thrombosis. This mAb is an antithrombotic agent that prevents platelet thrombosis without affecting intrinsic platelet function.

Animals↗
PubMed1986

von Willebrand's disease prevents occlusive thrombosis in stenosed and injured porcine coronary arteries.

We studied the role of von Willebrand factor in coronary thrombosis in normal, heterozygous, and homozygous von Willebrand's disease pigs by producing coronary stenosis with a Goldblatt clamp positioned around the left anterior descending coronary artery. Flow velocity was assessed by a 20-MHz Doppler velocity probe distal to the Goldblatt clamp. Myocardial extracellular potassium levels were measured by potassium-sensitive electrodes in myocardium supplied by the left anterior descending artery. Whereas stenosis sufficient to block reactive hyperemia to a 20-second occlusion produced an elevation of myocardial extracellular potassium, it produced neither spontaneous cyclic flow reductions nor permanent cessation of coronary blood flow velocity. Injury of the coronary artery at the stenosis site with spring-loaded forceps produced cyclic flow reductions or permanent cessation of flow in eight of nine phenotypically normal pigs. On the other hand, flow variations occurred in none of the 10 von Willebrand's disease pigs, including four given purified von Willebrand factor at a dose that failed to correct the bleeding time (p less than 0.001, chi 2 test). Permanent cessation of flow was caused by an occlusive platelet-fibrin-red-blood-cell thrombus. Scanning electron micrographs from pigs with cyclic flow variations and from von Willebrand's disease pigs showed injured endothelium covered by adherent platelets, red and white blood cells, and fibrin. These data suggest an important role of native von Willebrand factor in sudden occlusive arterial thrombosis following stenosis and intimal injury.

Animals↗
PubMedDate not supplied

von Willebrand factor and occlusive arterial thrombosis. A study in normal and von Willebrand's disease pigs with diet-induced hypercholesterolemia and atherosclerosis.

The thrombotic response of atherosclerotic arteries to stenosis and injury was studied in 14 pigs, eight normal and six with von Willebrand's disease (vWD). Atherosclerosis was produced by feeding a 1% to 2% cholesterol diet for 24 weeks. Both groups of pigs developed severe hypercholesterolemia, greater than five times baseline values. Coronary atherosclerosis was detected in all vWD pigs and in all but one normal pig and was not significantly different between groups. At sacrifice under general anesthesia, a Goldblatt clamp (GC) was positioned around the left anterior descending coronary (LAD) and carotid arteries to produce a stenotic segment, which was pinch-injured with needle holders. A 20 MHz Doppler velocity crystal was placed distal to the GC to detect cyclic flow reductions or permanent cessation of flow velocity indicative of occlusive thrombosis. In the phenotypically normal pigs with diet-induced atherosclerosis, occlusive thrombosis was detected in seven of seven LAD and seven of seven carotid arteries. In atherosclerotic vWD pigs, occlusive thrombosis failed to form in six LAD and 10 carotid arteries (p less than 0.003, Wilcoxon rank sum test). Scanning electron micrographs demonstrated platelet-fibrin microthrombi in both groups of pigs; only phenotypically normal pigs had occlusive thrombi. Von Willebrand factor is essential for the development of occlusive thrombosis and appears to support the progression of a mixed microthrombus to an occlusive thrombus.

Animals↗