Intravenous thrombolysis in refractory unstable angina pectoris.
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Angina, Unstable↗
Biomedical subjects
H V Anderson
Publications and source records attributed to H V Anderson.
Sixty-eight-year-old woman with intermittent hypoxemia.
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Aged↗
Diffuse vasospasm following stenting of a free gastroepiploic artery graft: resolution with balloon angioplasty and intensive medical therapy.
Vasospasm following balloon angioplasty of gastroepiploic artery bypass grafts can be prevented or reversed with vasodilators. In our patient, stent deployment for ostial stenosis of a free gastroepiploic artery graft was accompanied by severe, diffuse spasm and a change in graft configuration that required both intensive medical therapy and balloon angioplasty for resolution.
Angioplasty, Balloon, Coronary↗
Successful treatment of chronic total peripheral occlusions that failed conventional techniques using the stiff backend of the Glidewire.
The vast majority of failures of transcatheter interventions in patients with peripheral vascular disease are due to inability to cross the lesion with a guidewire. Although the use of the Glidewire has clearly improved the success rate, failures with especially chronic total occlusions still occur. We describe a new technique using the very stiff backend of the Glidewire, which we have found very successful, when conventional techniques fall in crossing highly resistant lesions.
Aged↗
One-year results of the Thrombolysis in Myocardial Infarction (TIMI) IIIB clinical trial. A randomized comparison of tissue-type plasminogen activator versus placebo and early invasive versus early conservative strategies in unstable angina and non-Q wave myocardial infarction.
OBJECTIVES: We report mortality, infarction, revascularization and repeat hospital admission events for 1 year after enrollment and randomization in the Thrombolysis in Myocardial Ischemia (TIMI) IIIB clinical trial. BACKGROUND: The purpose of this trial was to investigate the role of a thrombolytic agent added to conventional medical therapies and to compare an early invasive management strategy to a more conservative early strategy in patients with unstable angina and non-Q wave myocardial infarction. METHODS: There were 1,473 patients enrolled, and they received conventional anti-ischemic medical therapies. They were randomized to therapy with either tissue-type plasminogen activator (t-PA) or placebo and also to an early invasive management strategy with coronary arteriography at 18 to 48 h, followed by revascularization as soon as possible if appropriate, or, alternatively, to an early conservative strategy with arteriography and revascularization reserved for failure of initial therapy to prevent recurrent ischemia. The primary end point was a composite outcome variable and was assessed at 42 days. Patients were then managed entirely at the discretion of their treating physician. Follow-up contacts were made at 1 year. RESULTS: The incidence of death or nonfatal infarction for the t-PA- and placebo-treated groups was similar after 1 year (12.4% vs. 10.6%, p = 0.24). The incidence of death or nonfatal infarction was also similar after 1 year for the early invasive and early conservative strategies (10.8% vs. 12.2%, p = 0.42). A trial of this size should be able to detect differences in relative risk for death or infarction > or = 1.81 with a power of 80% at a significance level (alpha) of 0.01. Revascularization by 1 year was common, but was slightly more common with the early invasive than the early conservative strategy (64% vs. 58%, p < 0.001). This result was related entirely to a small difference in angioplasty rates (39% vs. 32%, p < 0.001) inasmuch as rates of bypass grafting by 1 year were equivalent (30% in each group, p = 0.50). The high rate of revascularization in both strategies was accompanied by comparable clinical status at the 1-year follow-up contact. CONCLUSIONS: In this large study of unstable angina and non-Q wave myocardial infarction, the incidence of death and nonfatal infarction or reinfarction was low but not trivial after 1 year (4.3% mortality, 8.8% nonfatal infarction). An early invasive management strategy was associated with slightly more coronary angioplasty procedures but equivalent numbers of bypass surgery procedures than a more conservative early strategy of catheterization and revascularization only for signs of recurrent ischemia. The incidence of death or nonfatal infarction, or both, did not differ after 1 year by strategy assignment, but fewer patients in the early invasive strategy group underwent later repeat hospital admission (26% vs. 33%, p < 0.001). Either strategy is appropriate for patient management; differences in hospital admissions and revascularization procedures, with their attendant costs, are likely to be minimal.
Adult↗
Coronary artery flow monitoring following coronary interventions.
Coronary guidewires with ultrasound transducer tips are commercially available and are appropriately sized for use in coronary interventions. These guidewires permit monitoring of coronary flow before, during and after the interventions. The measured flow signal contains valuable information regarding the quality and the stability of the final result. After completion of the procedure, monitoring the trend in average velocity over several minutes can reveal subtle alterations in flow that may presage abrupt closure. Abnormal or unstable flow patterns also may help predict lesions that might develop recurrences in the weeks and months after successful procedures.
Angioplasty, Balloon, Coronary↗
Coronary artery flow monitoring: the value of intravascular Doppler for detection of complications after interventions.
Ultrasound transducer-tipped guidewires can be used for coronary interventions, and they permit the monitoring of coronary flow before, during, and after the interventions. The flow signal contains valuable information regarding the quality and stability of the final result. Restoration of typical phasic flow patterns with diastolic predominance is one guide to final result. Monitoring the trend in average velocity over several minutes after completion of the procedure can detect subtle alterations in flow that may presage abrupt closure. These flow alterations might also help predict active plaques with heavy thrombus involvement that may undergo recurrence in the weeks and months after successful procedures.
Angioplasty, Balloon, Coronary↗
Role of angiography.
The role of coronary angiography in acute myocardial infarction is multifaceted. In the acute situation--for example, for primary angioplasty, suspected thrombolytic failure, or reocclusion--the goal of the angiographer should be therapeutic: to provide hemodynamic support, relieve ischemia, and interrupt the infarction process. In the nonacute or elective setting after infarction, the angiographer's goal should be to obtain diagnostic information only and not to approach the catheterization as a definitive therapeutic maneuver. This "uncoupling" of diagnostic angiography and revascularization is appropriate in light of the numerous trials discussed above. Either an invasive or a noninvasive approach to patient management can be justified with currently available data. The physician should not feel compelled to proceed with either approach necessarily. The patient's comfort level and the physician's comfort level with both approaches should be discussed by all concerned, when appropriate for the time constraints that exist with acute infarctions. Very likely, in the near future the two approaches, invasive and conservative, will undergo further analysis and modification as new agents and therapies become available.
Angioplasty, Balloon, Coronary↗
Transvalvular left ventricular assistance in cardiogenic shock secondary to acute myocardial infarction. Evidence for recovery from near fatal myocardial stunning.
OBJECTIVES: The purpose of this study was to test the hypothesis that transvalvular left ventricular assistance would support the circulation in patients with cardiogenic shock secondary to acute myocardial infarction and allow recovery of function in patients with a reversibly damaged (stunned) left ventricle. BACKGROUND: Cardiogenic shock occurs in 7.5% of patients presenting with acute myocardial infarction, resulting in survival of only 20%. Despite the use of aggressive interventional therapy in patients with shock secondary to anterior myocardial infarction, survival remains as low as 33%. METHODS: We studied 11 patients with acute myocardial infarction and cardiogenic shock, as defined by a cardiac index < 2 liters/min per m2, pulmonary capillary wedge pressure > 18 mm Hg and systolic blood pressure < 90 mm Hg during positive inotropic therapy. Patients were 57 +/- 13 years old (mean +/- SD) and had a mean left ventricular ejection fraction of 25 +/- 11%, mean arterial pressure of 69 +/- 13 mm Hg and mean cardiac index of 1.6 +/- 0.4 liters/min per m2 on admission to the study. RESULTS: During the 1st 24 h of left ventricular assistance, pulmonary capillary wedge pressure decreased from 26 +/- 4 to 16 +/- 4 mm Hg (p = 0.01), cardiac index increased from 1.6 +/- 0.4 to 2.4 +/- 0.4 liters/min per m2, and the dopamine hydrochloride dose decreased from 51 +/- 92 to 18 +/- 12 micrograms/kg body weight per min. In survivors, cardiac index improved to 3.2 +/- 0.5 liters/min per m2 (p = 0.01), and left ventricular ejection fraction improved to 34 +/- 5% (p < 0.05). The overall survival in the study group was 4 (36%) of 11 patients (95% confidence interval [CI] 8% to 65%), and 4 (66%) of 6 patients (95% CI 29% to 100%) with a Q wave anterior myocardial infarction survived. CONCLUSIONS: Transvalvular left ventricular support during cardiogenic shock complicating acute myocardial infarction is feasible and results in significant hemodynamic and functional improvement.
Female↗
Local effect of serotonin released during coronary angioplasty.
BACKGROUND: Serotonin is released after the aggregation of platelets, a phenomenon that may occur after coronary angioplasty. We sought to determine whether serotonin is released into the coronary circulation during coronary angioplasty and to assess whether serotonin can affect coronary-artery tone during angioplasty. METHODS: Blood samples were drawn from the ascending aorta and the coronary sinus of eight patients scheduled to undergo angioplasty of the left anterior descending or circumflex coronary artery. Samples were obtained before angioplasty and after each balloon dilation. The dimensions of arterial segments distal to the site of dilation were measured angiographically before angioplasty and 5 and 15 minutes after the last dilation in these eight patients and in seven similar patients; the latter group was treated with ketanserin, a serotonin2-receptor antagonist, before angioplasty. RESULTS: Before the eight patients underwent angioplasty, their mean (+/- SE) plasma serotonin level in the aorta was 2.5 +/- 0.7 ng per milliliter and that in the coronary sinus was 2.3 +/- 0.6 ng per milliliter (P = 0.34). The serotonin level in plasma from the coronary sinus rose significantly, to 31.5 +/- 13.5, 17.6 +/- 5.3, and 29.1 +/- 8.1 ng per milliliter after the first, second, and third dilations, respectively (P = 0.014 for the comparison with preoperative levels). In contrast, the serotonin level in plasma from the ascending aorta did not change. The cross-sectional area of the coronary artery was significantly reduced 5 and 15 minutes after the last dilation (from a preoperative value of 3.7 +/- 0.5 mm2 to 2.7 +/- 0.4 mm2 15 minutes after the last dilation; P = 0.011). This vasoconstriction was significantly blunted in the seven patients who received ketanserin (from 3.7 +/- 0.5 mm2 before angioplasty to 3.9 +/- 0.4 mm2 after 15 minutes) (P = 0.017 for comparison with the eight patients who did not receive ketanserin). CONCLUSIONS: Serotonin is released into the coronary circulation during angioplasty, and this vasoactive substance may contribute to the occurrence of vasoconstriction distal to the dilated site. The vasoconstriction is attenuated by ketanserin, a serotonin2-receptor antagonist.
Angioplasty, Balloon, Coronary↗
Cyclic flow variations after coronary angioplasty in humans: clinical and angiographic characteristics and elimination with 7E3 monoclonal antiplatelet antibody.
OBJECTIVES: We tested the hypothesis that cyclic alterations in coronary artery blood flow that occurred after coronary angioplasty could be attenuated or abolished by a monoclonal antibody to the platelet surface membrane GP IIb/IIIa receptor. BACKGROUND: Coronary artery cyclic flow variations may occur after coronary angioplasty in experimental animal models and humans. In animal models of coronary thrombosis, cyclic alterations in flow often have preceded thrombotic occlusion or reocclusion. Several agents that inhibit platelet function have been shown to attenuate or eliminate cyclic flow variations in these models. METHODS: We monitored coronary artery flow in 27 patients for 30 min after coronary angioplasty, using 0.018-in. (0.046 cm) coronary guide wires with pulsed wave Doppler ultrasound transducers on the distal tips. Clinical data were collected and quantitative analyses performed on coronary arteriograms made before and after the angioplasty procedures. We compared findings in patients with and without cyclic flow variations detected. RESULTS: There were 20 men and 7 women. Mean age was 58 years, and 63% had unstable angina. They received standard doses of nitrates, aspirin, heparin, calcium channel antagonists and other medications clinically indicated. Nevertheless, we detected cyclic flow variations in five patients (19%). Four of these patients had stable flow restored with intravenous injection of 0.25 mg/kg normal body weight of monoclonal antibody c7E3 Fab to the platelet GP IIb/IIIa receptor. In one patient, stable flow was restored by repeat dilation when an immediate angiogram revealed renarrowing. Patients developing cyclic alterations in flow had longer lesions (18.7 +/- 7.5 mm vs. 13.1 +/- 5.7 mm, p < 0.05) that had responded less well to angioplasty (stenosis postangioplasty 47 +/- 13% vs. 33 +/- 15%, p < 0.05). CONCLUSIONS: Cyclic alterations in coronary artery blood flow may occur in some patients after coronary angioplasty, despite the use of standard antiplatelet, antithrombotic and antivasospastic medications. We found that they could be eliminated by this monoclonal antibody that blocks the final common event of platelet aggregation.
Abciximab↗
Spontaneous coronary arterial dissection causing acute myocardial infarction.
We report the case of a middle-aged female who presented with an acute inferior myocardial infarction treated with intravenous thrombolytics. Immediate coronary angiography demonstrated the presence of a spiral dissection and a large thrombus. After 1 week of anticoagulation the thrombus had resolved, but a large spiral dissection persisted. This was confirmed by intracoronary ultrasound. We then review the literature on spontaneous coronary arterial dissection.
Aortic Dissection↗
Clopidogrel is more effective than aspirin as adjuvant treatment to prevent reocclusion after thrombolysis.
Clopidogrel is a thienopyridine derivative and a potent inhibitor of ADP-induced platelet aggregation. We compared clopidogrel with aspirin as an adjunctive treatment to tissue-type plasminogen activator (t-PA) for thrombolysis and reocclusion. Thrombosis was induced in coronary arteries of 32 dogs by injuring the endothelium with an electric charge. Coronary blood flow velocity was monitored by a pulsed Doppler flow probe placed around the artery. After the artery had been occluded by a thrombus for 3 continuous hours, each animal was given one of the following intravenous treatments: 1) t-PA (80 micrograms/kg + 8 micrograms.kg-1.h-1) and heparin (200 U/kg) (group 1, n = 7); 2) t-PA, heparin, and aspirin (5 mg/kg) (group 2, n = 8); 3) t-PA, heparin, and clopidogrel (5 mg/kg) (group 3, n = 9); and 4) t-PA, heparin, and clopidogrel (10 mg/kg + 2.5 mg.kg-1.h-1) (group 4, n = 8). After treatment, thrombolysis developed in 45 +/- 12 min in group 1, 39 +/- 10 min in group 2, 39 +/- 10 min in group 3, and 27 +/- 10 min in group 4 (compared with group 1, P > 0.05). After thrombolysis, reocclusion occurred in 5 of 5 dogs in group 1 and 7 of 7 in group 2, but only 2 of 7 in group 3 and none of 7 in group 4 (compared with groups 1 and 2, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Liposome-bound prostaglandin E1 often prevents cyclic flow variations in stenosed and endothelium-injured canine coronary arteries.
BACKGROUND: Prostaglandin E1 is a potent vasodilator with anti-inflammatory and antiplatelet effects. We tested the hypothesis that prostaglandin E1 attenuates or prevents platelet aggregation-associated cyclic flow variations (CFVs) in severely stenosed and endothelium-injured coronary arteries. METHODS AND RESULTS: We induced CFVs in 21 dogs by placing an external constrictor around the left anterior descending coronary artery at the site where the endothelium had been mechanically injured. The blood flow velocity in the artery was monitored by a pulsed Doppler flow probe. Sixty minutes after CFVs were established, liposome-bound prostaglandin E1, a stable formulation, was administered intravenously to 12 dogs at incremental doses of 0.25, 0.5, 1, and 2 micrograms/kg body wt; it abolished CFVs in 8 of the 12 dogs (67%). After CFVs were eliminated, epinephrine was infused intravenously, and at a dose of 6.6 +/- 1.6 micrograms/min, it restored CFVs in 7 of 7 dogs. Control dogs (n = 9) were treated with free prostaglandin E1, which did not abolish CFVs in any dog. CONCLUSIONS: Liposome-bound but not free prostaglandin E1 effectively diminishes CFVs in severely stenosed and endothelium-injured canine coronary arteries.
Alprostadil↗
Blockade of platelet membrane glycoprotein Ib receptors delays intracoronary thrombogenesis, enhances thrombolysis, and delays coronary artery reocclusion in dogs.
Von Willebrand factor and platelet membrane glycoprotein Ib receptors interact to mediate platelet adhesion and thrombogenesis in stenosed and endothelium-injured arteries. We wished to determine whether blocking glycoprotein Ib receptors with a recombinant von Willibrand factor binding domain (VCL) increases the time required for thrombus formation after injury to the coronary arteries. We also wished to determine whether, after thrombolysis with tissue plasminogen activator (TPA), VCL delays or protects against coronary artery reocclusion. Twenty-seven dogs were treated with either saline, VCL, or aspirin before thrombosis was induced in their coronary arteries by electrical injury. The time from injury to the formation of occlusive thrombi was significantly greater with VCL (70 +/- 10 minutes) and aspirin (69 +/- 20 minutes) than with saline (18 +/- 3 minutes, P < .001 and P < .05). Thrombosis was induced in 30 other dogs that then received thrombolytic treatment in four groups. Our major finding was that coronary artery reocclusion occurred in 72 +/- 11 minutes after treatment with TPA (80 micrograms/kg + 8 micrograms.kg-1.min-1) and heparin (200 U/kg) (n = 7); in 142 +/- 24 minutes after TPA, heparin, and VCL (4 mg/kg + 2 mg.kg-1.h-1) (n = 7) (compared with TPA and heparin, P < .05); in 74 +/- 13 minutes after TPA, heparin, and aspirin (5 mg/kg) (n = 8); and in 173 +/- 8 minutes after TPA, heparin, VCL, and aspirin (n = 8) (compared with TPA and heparin, P < .001). Thus, VCL increases the length of time required for thrombus formation in coronary arteries, and, when given with TPA and heparin, delays coronary artery reocclusion more effectively than aspirin.
Animals↗
Thrombolysis in acute myocardial infarction.
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Angioplasty, Balloon, Coronary↗
Coronary artery flow monitoring following coronary interventions.
Technologic innovations have made it possible to measure coronary artery blood flow in awake patients. Both flow velocity as well as flow reserve can be assessed. In particular, the period of time immediately following coronary interventions offers a unique opportunity to study important features of coronary flow behavior. In 22 patients, coronary flow reserve was measured before and after an intervention, either angioplasty or atherectomy, using a 0.018-in Doppler guidewire (Flowire). The minimum lumen diameter (MLD) was increased from 1.0 +/- 0.4 to 1.7 +/- 0.4 mm, while coronary flow velocity increased significantly, rising from 29 +/- 13 to 39 +/- 14 cm/sec (p < 0.025). The maximum hyperemic velocity also increased, from 44 +/- 16 to 69 +/- 21 cm/sec. Using only the preintervention or postintervention values, the flow reserve ratio was 1.53 +/- 0.4 prior to intervention and 1.84 +/- 0.5 after intervention (p = nonsignificant). However, the post-intervention value may have been artifactually reduced by the fact that both resting as well as hyperemic velocities increased. When the post-intervention flow reserve ratio was recalculated, using the preintervention resting value, flow reserve ratio was seen in increase from 1.53 +/- 0.4 to 2.73 +/- 1.2 (p < 0.001). Measurements of coronary flow in the postintervention period also revealed several interesting phenomena. Spasm of a coronary artery was documented, and its resolution in response to intracoronary nitroglycerin was observed. Elastic recoil following angioplasty was documented by gradual decline in coronary flow over 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)
Angioplasty, Balloon, Coronary↗
Restenosis after coronary angioplasty.
Coronary angioplasty is used to treat coronary disease in many patients. Indications for angioplasty have expanded since it was first performed, mainly as a result of improvement in equipment and techniques. One problem with coronary angioplasty is the phenomenon of renarrowing of the treated coronary lesion, a process called restenosis. The events that constitute restenosis appear to be a universal response to the arterial wall injury of angioplasty. They are currently characterized as follows: platelet adhesion and aggregation on the damaged endothelium and within deep splits into the tunica media; release of platelet-derived growth factors; inflammation of the mechanically injured medial zone; transformation of smooth muscle cells of the tunica media after their activation by several of the growth-promoting substances; migration and proliferation of transformed smooth muscle cells, with secretion of copious amounts of extracellular matrix material; and, finally, termination of the growth process with regrowth of endothelium over the injured area. A decade of research work has helped identify clinical correlates of restenosis after coronary angioplasty procedures. This work is hindered by lack of a uniform angiographic definition of restenosis. In addition, much of the information has come from small studies, with incomplete follow-up and retrospective orientation. Nevertheless, some data are available. Patient-related correlates include male gender, unstable angina, diabetes, and continued smoking after angioplasty. Lesion-related correlates include multilesional and multivessel procedures, higher postangioplasty residual stenosis, proximal vessel location, location in the left anterior descending artery, location in a vein graft, long lesions, and total occlusions. The only consistent procedure-related correlate has been incorrect sizing of the angioplasty balloon to the treated artery. For the purposes of individual patient care, clinical correlates are not helpful. No group of variables has been found to be associated with complete freedom from restenosis, and no group is completely predictive of restenosis. All patients undergoing angioplasty procedures require some follow-up through subsequent months and years. Symptom status and the results of noninvasive studies have been investigated for purposes of follow-up. Symptoms are virtually useless by themselves for predicting restenosis or its absence. When symptom status is combined with exercise thallium 201 scintigraphy performed 4 to 6 months after an angioplasty procedure, the two factors are less than ideal but have a negative predictive value of more than 90%. This means that more than 90% of patients who have neither symptoms nor evidence of ischemia by thallium 201 scintigraphy will not have angiographic restenosis.(ABSTRACT TRUNCATED AT 400 WORDS)
Angioplasty, Balloon, Coronary↗