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Biomedical subjects

J J Ferguson

Publications and source records attributed to J J Ferguson.

At least 109 records · Page 6Linked to original sources
PubMed1992

Activated clotting times and activated partial thromboplastin times in patients undergoing coronary angioplasty who receive bolus doses of heparin.

The accurate assessment of coagulation status is an important part of interventional procedures performed in the cardiac catheterization laboratory. While the traditional clinical means of assessing heparin anticoagulation has been with the activated partial thromboplastin time (APTT), the activated coagulation time (ACT) has come into widespread use in the catheterization laboratory as an assay of whole blood clotting time which can be performed rapidly at the bedside. The purpose of the present study was to (1) assess the anticoagulant effect of a 10,000 U bolus of heparin in PTCA patients and (2) document the relationship between ACTs and APTTs in a subset of these patients. Baseline and postheparin ACTs were measured using a HemoTec coagulation timer in 545 unselected PTCA patients. The average baseline ACT was 120 +/- 22 sec. After a 10,000 U bolus of heparin the average ACT was 249 +/- 44 sec; 58% of patients had an ACT less than 250 sec, 17% had an ACT between 250 and 275 sec, 12% had an ACT between 275 and 300 sec, and 13% had an ACT greater than 300 sec. A total of 175 paired ACT and APTT measurements were obtained in a random subset of these patients at baseline, after heparinization, and at 4-6 hr intervals after the procedure. The APTT was limited by absolute upper and lower limits of 150 and 22 sec; there were no such limits on the ACT. When limiting values were excluded, there was a strong overall correlation between ACT and APTT measurements (r = 0.92, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Endogenous nitric oxide protects against platelet aggregation and cyclic flow variations in stenosed and endothelium-injured arteries.

BACKGROUND: This study was designed to test the hypothesis that endogenously produced nitric oxide protects against platelet aggregation and cyclic flow variations in stenosed and endothelium-injured arteries of mongrel dogs. METHODS AND RESULTS: NG-Monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation, was administered at 5 mg/kg to 15 dogs after the left anterior descending coronary artery was mechanically injured and narrowed by external constrictors and to nine dogs before endothelial injury of the femoral artery and after injury and moderate arterial constriction. Treatment with L-NMMA resulted in cyclic flow variations (as detected by external Doppler flow probes) in the left anterior descending artery of seven of 15 dogs and in the femoral artery of four of nine dogs after endothelial injury. L-Arginine, the precursor for nitric oxide synthesis, was administered at 60 mg/kg and abolished cyclic flow variations in each of the 11 dogs. D-Arginine did not change the L-NMMA-induced cyclic flow variations. Saline infusion did not induce or change cyclic flow variations in any of the animals. Acetylcholine (1, 10, and 100 micrograms/min; n = 9) was administered in the femoral artery of nine additional dogs before and after endothelial injury in moderately stenosed femoral arteries. Acetylcholine did not induce cyclic flow variations in any animal; however, it did increase the severity of cyclic flow variations that developed in severely stenosed arteries. The diameter of the femoral artery was measured by intravascular ultrasound imaging. L-NMMA caused vasoconstriction of normal arteries, but no change was detected in endothelium-injured arteries. In contrast, L-arginine caused vasodilation of normal arteries, but, again, no change was noted in endothelium-injured arteries. Acetylcholine dilated normal femoral arteries but constricted arteries with endothelial injury. In both in vitro and ex vivo platelet studies, L-NMMA enhanced platelet aggregation, whereas L-arginine significantly reduced platelet aggregation. D-Arginine and acetylcholine showed no effect on platelet aggregation. CONCLUSIONS: Promotion of nitric oxide production decreases platelet aggregation and may eliminate cyclic flow variations, whereas a reduction in nitric oxide formation enhances platelet aggregation and may induce cyclic flow variations. Acetylcholine causes vasoconstriction at the femoral arterial site of endothelial injury and may increase the severity of cyclic flow variations.

Acetylcholine↗
PubMed1992

Combination of inhibition of thrombin and blockade of thromboxane A2 synthetase and receptors enhances thrombolysis and delays reocclusion in canine coronary arteries.

BACKGROUND: The efficacy of thrombolytic therapy in treating patients with acute myocardial infarction is limited by failure to achieve reperfusion in some patients, by the prolonged time required to achieve reperfusion, and by reocclusion of some coronary arteries. We designed this study to examine the effect of combined inhibition of thrombin and thromboxane synthesis and blockade of thromboxane A2 receptors in addition to tissue-type plasminogen activator (t-PA) on thrombolysis and reocclusion in an experimental canine model with coronary thrombosis. METHODS AND RESULTS: Blood flow velocity in the left anterior descending coronary artery (LAD) of 32 anesthetized mongrel dogs was monitored by a pulsed Doppler flow probe. Coronary thrombosis was induced by applying electrical stimulation to the LAD at the site where an external constrictor was used to narrow the artery. Three hours after the formation of occlusive thrombus, animals were randomly assigned to receive one of the following: 1) t-PA (80 micrograms/kg + 8 micrograms.kg-1.min-1 i.v.) and saline; 2) t-PA and hirulog, a hirudin-based synthetic peptide and specific thrombin inhibitor (2 mg/kg + 2 mg.kg-1.hr-1 i.v.); 3) t-PA and ridogrel, a combined thromboxane A2 synthetase inhibitor and receptor antagonist (5 mg/kg + 2.5 mg.kg-1.hr-1 i.v.); or 4) t-PA, hirulog, and ridogrel. Reperfusion developed in 14% (one of seven) of dogs treated with t-PA alone at an average of 86 +/- 4 minutes after treatment, in 78% (seven of nine) of dogs treated with t-PA plus hirulog at 53 +/- 11 minutes, in 13% (one of eight) of dogs treated with t-PA plus ridogrel at 85 +/- 5 minutes, and in 88% (seven of eight) of dogs treated with t-PA, hirulog, and ridogrel at 37 +/- 10 minutes (comparison of the frequency of and the time to reperfusion, both p < 0.01). Among the dogs with reestablished coronary blood flow, reocclusion developed in the one treated with t-PA alone at 36 minutes after reperfusion, in seven of the seven treated with t-PA plus hirulog at 66 +/- 15 minutes, and in two of the seven treated with t-PA, hirulog, and ridogrel at 151 +/- 21 minutes (comparison of the frequency of and time to reocclusion, both p < 0.05). Reocclusion was not detected in the one dog treated with t-PA and ridogrel or in the other five dogs treated with t-PA, hirulog, and ridogrel within 180 minutes after reperfusion. Hirulog prolonged and maintained activated clotting times at a level twice that of baseline values. Hirulog inhibited ex vivo platelet aggregation induced by thrombin, and ridogrel inhibited platelet aggregation induced by U46619, a thromboxane mimetic. CONCLUSIONS: Inhibition of thrombin in addition to treatment with t-PA enhances thrombolysis. A combination of inhibition of thrombin and thromboxane synthetase and blockade of thromboxane A2 receptor enhances thrombolysis and delays or may prevent reocclusion of the recanalized coronary arteries.

Animals↗
PubMed1992

Should all patients with risk factors for ischemic heart disease receive aspirin?

Unstable angina appears to be caused by relatively brief, repetitive episodes of myocardial oxygen impairment secondary to platelet aggregation and dynamic vasoconstriction at sites of coronary stenosis and endothelial injury. With chronic endothelial injury, the accumulation of thromboxane A(2), serotonin, and other mediators may contribute to platelet aggregation and dynamic vasoconstriction. Aspirin acetylates the platelet enzyme, cyclooxygenase, thereby inhibiting the formation of thromboxane A(2). In certain patients with unstable angina, 1 to 4 aspirin tablets per day has proved beneficial in reducing the risk of myocardial infarction and death. Moreover, combining aspirin with a selected thrombolytic agent, such as streptokinase, appears to potentiate thrombolysis and further reduce mortality. Aspirin's toxicity to the gastrointestinal tract and its tendency to decrease vascular concentrations of prostacyclin, a local endothelial factor that hinders thrombogenesis and promotes endogenous vasodilation, are concerns when used in long-term treatment; for this reason, we do not recommend aspirin therapy for every patient with an acute coronary syndrome. We do, however, advocate such therapy for those with unstable angina and, in combination with selected thrombolytic interventions, for those with acute Q-wave myocardial infarctions in whom aspirin is not contraindicated.

Editorial↗
PubMed1992

Balloon mitral valvuloplasty: clinical experience at the Texas Heart Institute.

For treatment of symptomatic mitral valve stenosis, balloon valvuloplasty has emerged as an alternative to surgery. This report describes our initial clinical experience with balloon mitral valvuloplasty in 45 patients (37 women and 8 men; age range, 34 to 79 years) treated from December 1986 through March 1991. Thirty-nine of the 45 patients (87%) underwent a complete procedure (that is, they had at least 1 balloon inflation and did not require emergency surgery). Pre- and post-procedural catheterization showed that these patients had a significant improvement in mean mitral valve area, from 1.0 +/- 0.3 cm(2) to 1.9+/-0.8 cm(2). Catheterization data revealed a decrease in transmitral gradient, from 16.3 +/- 7.6 mmHg to 7.6 +/- 3.7 mmHg, and an increase in cardiac index, from 2.5 +/- 0.7 L/min/m(2) to 2.9 +/- 0.8 L/min/m(2). These improvements were all statistically significant (p <0.0005). A clinically successful balloon mitral valvuloplasty was defined as an uncomplicated procedure yielding either a final mitral valve area > 1.5 cm(2) or a 40% increase in mitral valve area, and an immediate post-valvuloplasty mitral regurgitation grade </=3+. Thirty-two of the 45 patients (71%) were considered to have had a successful procedure. Another 7 patients underwent subsequent mitral valve replacement due to either a suboptimal final mitral valve area (3 patients) or >2+ increase in mitral regurgitation (4 patients). In 6 patients, the procedure was considered incomplete because of technical failure or complications. Two of these patients had nonfatal cardiac tamponade, and 1 had a torn mitral annulus that resulted in severe mitral regurgitation requiring emergent mitral valve replacement. In another patient, we were unable to cross the mitral valve with a 2nd valvuloplasty balloon after the 1st one proved unsatisfactory. There were 2 in-hospital deaths, only 1 of which was related to the procedure. Over time, our success rate has improved from 60% in the 1st 20 patients to 80% in the subsequent 25 patients, reflecting a learning curve. In particular, we attribute this improvement to increased operator experience, refinements in balloon technology, and, in more recent procedures, the initial use of smaller balloons. The improvement also reflects a change in demographic pattern, characterized by recent application of the procedure to younger patients with fewer concomitant illnesses. Because long-term follow-up data are available for only 23 patients, we cannot comment on the long-term efficacy of this technique. Overall, however, our short-term experience indicates that balloon mitral valvuloplasty is a safe, effective alternative for treating symptomatic mitral valve stenosis in carefully selected adults.

Journal Article↗
PubMed1992

Total arterial compliance: differences between spontaneously hypertensive rats and normotensive Wistar-Kyoto rats.

Invasive hemodynamic measurements were performed on 14 normotensive Wistar-Kyoto (WKY) rats and 15 spontaneously hypertensive rats (SHRs) to test the hypothesis that SHRs have lower total arterial compliance than WKY rats. Ascending aortic pressure was measured with a catheter-tip manometer, and aortic flow was measured with an electromagnetic flow probe. Prolonged diastoles were produced by an electrocardiographically timed aortic occluder. The aortic decay time constant (Tau) for each prolonged diastole was calculated by an exponential fit of the initial linear segment of the log (pressure)-time curve. Tau is the product of resistance (R) and compliance (C) in the Windkessel model for the arterial system. Total arterial compliance was therefore determined from the relation Tau/R. The total arterial compliance index was calculated by correcting for body weight. Compliance was also estimated by the stroke volume/pulse pressure ratio. Compared with WKY rats, SHRs have higher mean pressure (111 +/- 19 [SD] mm Hg vs 71 +/- 14, P less than .0001), higher mean flow (0.50 +/- 0.10 mL/sec vs 0.38 +/- 0.04, P less than .001), and a shorter decay time constant (365 +/- 54 msec vs 475 +/- 54, P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Regional myocardial blood flow and left ventricular diastolic properties in pacing-induced ischemia.

The relation between left ventricular diastolic abnormalities and myocardial blood flow during ischemia was studied in eight open chest dogs with critical stenoses of the proximal left anterior descending and circumflex coronary arteries. The heart was paced at 1.7 times the heart rate at rest for 3 min. In dogs with coronary stenoses, left ventricular end-diastolic pressure increased from 8 +/- 1 to 14 +/- 2 mm Hg during pacing tachycardia (p less than 0.01) and 16 +/- 3 mm Hg (p less than 0.01) after pacing, with increased end-diastolic and end-systolic segment lengths in the ischemic regions. Left ventricular diastolic pressure-segment length relations for ischemic regions shifted upward during and after pacing tachycardia in dogs with coronary stenoses, indicating decreased regional diastolic distensibility. In dogs without coronary stenoses, the left ventricular diastolic pressure-segment length relation was unaltered. Pacing tachycardia without coronary stenoses induced an increase in anterograde coronary blood flow (assessed by flow meter) in both the left anterior descending and circumflex coronary arteries, and a decrease in regional vascular resistance. In dogs with coronary stenoses, regional vascular resistance before pacing was decreased by 18%; myocardial blood flow (assessed by microspheres) was unchanged in both the left anterior descending and circumflex coronary artery territories. During pacing tachycardia with coronary stenoses, regional coronary vascular resistance did not decrease further; subendocardial myocardial blood flow distal to the left anterior descending coronary artery stenosis decreased (from 1.03 +/- 0.07 to 0.67 +/- 0.12 ml/min per g, p less than 0.01), as did subendocardial to subepicardial blood flow ratio (from 1.04 +/- 0.09 to 0.42 +/- 0.08, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Twelve-lead electrocardiographic evaluation of ischemia during percutaneous transluminal coronary angioplasty and its correlation with acute reocclusion.

The sensitivity of the surface 12-lead electrocardiogram and that of standard (limb-lead) monitoring for the detection of ischemia during percutaneous transluminal coronary angioplasty were compared in 115 patients. The purpose was to identify the electrocardiographic leads that provide the most sensitive indicators of coronary ischemia during percutaneous transaluminal coronary angioplasty and to evaluate the "ischemic fingerprint" that is obtained with 12-lead electrocardiogram during balloon inflation as a predictor of abrupt reocclusion after successful percutaneous transaluminal coronary angioplasty procedures. During balloon inflations of 30 seconds, ischemia was detected in 61 of 145 vessels (42%) by limb-lead monitoring alone versus 130 of 145 vessels (90%) by 12-lead electrocardiography (p less than or equal to 0.001). In the nine patients (7.8%) who experienced abrupt reocclusion within 24 hours, the electrocardiogram during chest pain after percutaneous transaluminal coronary angioplasty was identical to that obtained during percutaneous transaluminal coronary angioplasty ("ischemic fingerprint"). None of the six patients who had chest pain after percutaneous transaluminal coronary angioplasty without evidence of abrupt reocclusion reproduced their ischemic fingerprint. The suggested optimal leads for monitoring ischemia are as follows: left anterior descending coronary artery, V2, and V3; circumflex artery, V2, and V3; and right coronary artery, III and aVF.

Adult↗
PubMed1991

Efficacy of multiple balloon aortic valvuloplasty procedures. The Mansfield Scientific Aortic Valvuloplasty Registry Investigators.

To determine the efficacy of a second balloon aortic valvuloplasty procedure in comparison with the original procedure, 47 patients (18 men, 29 women; mean age 77 +/- 10 years) who underwent two balloon aortic valvuloplasty procedures over a mean interval of 6.4 months between procedures (range 2 days to 15 months) were retrospectively examined. The mean pressure gradient across the aortic valve was significantly higher before the first than before the second valvuloplasty procedure (62 +/- 21 vs. 53 +/- 21 mm Hg; p less than 0.05) and after the first compared with after the second procedure (32 +/- 13 vs. 28 +/- 14 mm Hg; p less than 0.05). The cardiac output and stroke volume after the first procedure were significantly greater than the values for these variables after the second procedure (4.4 +/- 1.1 vs. 3.8 +/- 1.1 liters/min; p less than 0.05; and 54 +/- 17 vs. 47 +/- 15 ml/beat; p less than 0.05, respectively). There were no significant differences in the change observed in any variable between the first and second procedures. At a mean follow-up interval of 5.3 months (range 6 days to 15 months) after the second procedure 18 (38%) of the 47 patients had died, 12 (25%) required surgical valve replacement and 4 (8%) required a third valvuloplasty procedure. Overall, 31 (66%) of 47 patients met clinical failure end points after the second procedure. Three patients had two failure end points. The 47 patients were divided into two groups on the basis of the interval between valvuloplasty procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Doppler echocardiography in 180 normally functioning St. Jude Medical aortic valve prostheses. Early and late postoperative assessments.

Limited Doppler echocardiographic data are available regarding velocities and gradients across normally functioning St. Jude Medical valves in the aortic position. To establish a standard reference for Doppler characteristics of normal aortic St. Jude Medical prostheses, we recorded continuous-wave Doppler measurements of peak and mean velocities and peak and mean gradients in 180 patients with normally functioning St. Jude aortic valves. There were 119 men and 61 women in the study; the mean age was 57 years. Minimal valvular regurgitation was present in 56 patients (31 percent). Velocities and gradients were reported in five patient groups according to valve sizes of 19 mm, 21 mm, 23 mm, 25 mm, and 27 mm; the mean gradients were 16 +/- 6, 16 +/- 6, 14 +/- 5, 12 +/- 5, and 12 +/- 6, respectively. Differences in velocities and gradients among the five valve sizes were not statistically significant (p = 0.05). Velocities and gradients were also analyzed in three patient groups according to time intervals after valve replacement. The first group (n = 64) underwent Doppler evaluation one to seven days postoperatively (mean, six days); the second group (n = 60) was evaluated after 8 to 30 days postoperatively (mean, 12 days); and the third group (n = 56) was evaluated after more than 30 days postoperatively (mean, 691 days). There were no significant differences in measurements for the three groups.

Aortic Valve↗
PubMed1991

Unstable angina pectoris and the progression to acute myocardial infarction. Role of platelets and platelet-derived mediators.

The conversion from stable to unstable angina and the further progression to myocardial infarction are usually associated with atherosclerotic plaque fissuring or ulceration at sites of coronary artery stenosis and subsequent development of a thrombus. This thrombus formation is initiated by platelet adhesion and aggregation; these, in turn, are promoted by the local release and accumulation of thromboxane A(2) and serotonin. This accumulation and the resulting platelet aggregation at sites of endothelial injury cause dynamic vasoconstriction. With time, the platelet-initiated thrombus expands to include white and red blood cells in a fibrin mesh. Thus, a fully occlusive coronary thrombus may develop and cause the progression from unstable angina to acute myocardial infarction, often Q-wave myocardial infarction. We believe that the connection between unstable angina and acute myocardial infarction is a continuum relative to the processes of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary stenosis lasts only a few minutes and is repetitive, unstable angina or non-Q wave myocardial infarction occurs. However, when complete coronary artery occlusion lasts for longer than 4 hours, a transmural or Q-wave myocardial infarction results. Recently, in experimental animal models with mechanically induced coronary artery stenoses and endothelial injury, we have found that other mediators, including adenosine diphosphate and thrombin, also contribute to coronary artery thrombosis. Moreover, in humans with limiting angina, we have identified spontaneous coronary blood flow variations in a pattern similar to the variations caused by alternating platelet attachment and dislodgement in experimental canine modes. In this review, we add information to our previous observations in order to present the possible mechanisms of conversion from chronic to acute coronary heart disease syndromes.

Journal Article↗
PubMed1991

Documentation of experimentally induced thrombus formation using intravascular ultrasound.

The purpose of the present study is to assess the ability of intravascular ultrasound to detect acute dynamic thrombus formation in canine blood vessels with damaged endothelium. Ultrasound catheters (20 MHz) were placed in the femoral arteries of anesthetized dogs, and imaging transducers were positioned at the sites of external constrictors applied to areas of endothelial injury. Flows were measured with externally applied Doppler crystals placed proximal to the constrictors. Twenty experimental procedures were performed in 18 dogs. Four procedures were performed using the InterTherapy system (4.9 Fr catheters) and 16 procedures were performed using the Boston Scientific/Diasonics system (6.0 and 4.8 Fr catheters). After injuring the endothelium by rubbing the adventitial surface with cushioned forceps, we placed the constrictors and catheters and found that femoral blood flow usually decreased to zero or near-zero over a 3- to 4-minute period. Striking the exposed artery dislodged the obstruction seen on the intravascular ultrasound images and restored flow to normal; spontaneous increases in flow associated with a reopening of the lumen were also noted. After femoral arterial blood flow returned to normal, another cycle of decreasing flow and thrombus formation was spontaneously initiated. Intravascular ultrasound images of thrombus formation were obtained in 18 of 20 experimental procedures, all associated with zero or near-zero arterial flow. Images obtained during spontaneous decreases in femoral artery flow demonstrated the gradual accumulation of material on the lumen. The obstructing thrombus had distinct borders and a "speckled" appearance on ultrasound, especially on dynamic images, which became increasingly bright and uniform with time. At the end of each procedure, the arterial segments were removed for histologic analysis. Gross thrombus was visible in all cases. Therefore, in this experimental model, intravascular ultrasound can successfully detect both the acute formation of thrombus associated with spontaneous episodes of decreased flow and the resolution of thrombus within injured and narrowed femoral arteries. Fresh thrombus has a unique ultrasound pattern that evolves gradually over time.

Journal Article↗
PubMed1990

Balloon aortic valvuloplasty: the Texas Heart Institute experience.

Between October 1986 and January 1989, 73 percutaneous catheter balloon aortic valvuloplasty procedures were performed in 68 adult patients (32 men and 36 women; mean age, 77 +/- 9 years) with severe symptomatic aortic stenosis. Following the procedures, significant improvements were documented in aortic valve area, mean transvalvular pressure gradient, peak-to-peak pressure gradient, left ventricular systolic pressure, radionuclide ejection fraction, and left ventricular end-systolic volume index. There were no procedure-related deaths, but 2 patients (3%) required emergency surgery for acute aortic regurgitation. During hospitalization, 4 patients had persistent symptoms (3 died; 1 subsequently underwent repeat valvuloplasty and later, valve replacement). Short-term clinical improvement was noted in 59 of 65 patients (91%). During the follow-up period (mean, 11.6 +/- 8.4 months), 22 patients died (including the 3 who died during hospitalization). Sixteen underwent aortic valve replacement (including the 2 who underwent emergency aortic valve replacement); all 16 are alive. A total of 6 patients (1 with an initial balloon aortic valvuloplasty at an outside institution) underwent repeat valvuloplasty; of those, 4 subsequently underwent aortic valve replacement, and 2 died. Of the remaining 30 patients, 27 continue to experience relief of symptoms, and 3 have clinical symptoms that have not improved or have worsened since the valvuloplasty procedure. Multivariate predictors of clinical outcome (p<0.05) included post-valvuloplasty aortic valve area, pre- and post-valvuloplasty ejection fraction, absence of coronary artery disease, and absolute change in valve area. Overall actuarial and event-free survivals were 83% and 49%, respectively, at 1 year. Although clinical improvement is frequently noted after balloon aortic valvuloplasty, the procedure is associated with a high recurrence of symptoms and restenosis. Balloon aortic valvuloplasty is at best a palliative procedure; when feasible, surgical valve replacement is the more definitive therapy.

Journal Article↗
PubMed1990

The use of temporary transvenous pacing catheters during percutaneous transluminal coronary angioplasty.

The use of temporary transvenous pacemakers during percutaneous transluminal coronary angioplasty (PTCA) over a 7(1/2)-month period at our institution was studied retrospectively. During that time, 379 patients underwent PTCA with temporary prophylactic pacemakers in place; 398 patients underwent PTCA without prophylactic pacemakers. We examined factors such as the necessity for emergent pacemaker placement, frequency of pacing during angioplasty, indications for pacing, effectiveness of the type of pacemaker inserted, and complications associated with pacemaker placement. Pacing was indicated in 40 of the 379 patients with prophylactic pacemakers; in only 1 of the 398 patients without prophylactic pacemakers was emergent pacing required for hemodynamic instability. In the patients with prophylactic pacemakers, pacing was initiated during the procedure for 32 patients with transient hemodynamically insignificant bradycardia, 3 patients with sustained bradycardia or heart block, and 5 patients with acute vessel occlusion and associated hypotension or bradycardia, or other episodes of hemodynamic instability. Thus, in only 8 of the 379 patients was pacing instituted for something other than hemodynamically insignificant bradycardia, and in only 5 of the 379 patients was it initiated for hemodynamic instability. The overall incidence of pacing for hemodynamic instability was 6 of 777 (0.8%). The pacing catheters inserted (379 prophylactic and 1 emergent) include #7 Pacewedge (42%), #6 bipolar (29%), #7 Myler (18%), and #7 Zucker (11%). Pacing thresholds were tested in 300 patients. The Pacewedge balloon-tipped pacing catheters had a significantly higher (p < 0.001) pacing threshold for right ventricular capture than the other (non-balloon) pacing catheters used. Two cases of sustained ventricular dysrhythmia were attributed to placement of stiff pacing catheters. No other pacemaker-related complications occurred. From these data we conclude that although there are few complications associated with the prophylactic placement of pacing catheters for PTCA, the need for cardiac pacing for hemodynamic instability during PTCA is low.

Journal Article↗
PubMed1990

Phonocardiographic assessment of hemodynamic response to balloon aortic valvuloplasty.

The time to systolic murmur peak is a clinical index that is useful in assessing the severity of valvular aortic stenosis. To determine whether phonocardiography could be used to detect a change in the timing of the murmur and thus to measure hemodynamic improvements in elderly balloon aortic valvuloplasty patients, we retrospectively reviewed phonocardiographic tracings of 18 patients taken before and after the procedure. Ten men and 8 women were included in the study; the mean age was 80.7 +/- 11.2 years (range, 64 to 90). Phonocardiographic signals were digitized, and the R-wave to murmur peak interval (R-MP) was measured. In 11 patients, the R-MP decreased (mean decrease, 16% +/- 11%): of these, 10 had a significant (> 25%) decrease in mean gradient; 10 had a significant (> 25%) decrease in peak-to-peak gradient; and the average increase in aortic valve area was 38%. Seven patients had an increase in R-MP (mean increase, 10% +/- 9%): of these, 6 had a decrease in mean gradient of less than 25%; 6 had a decrease in peak-to-peak gradient of less than 25%; and the average increase in aortic valve area was 21%. Pre- and post-balloon aortic valvuloplasty heart rates were not significantly different (71 +/- 8 beats/min versus 73 +/- 5 beats/min). In this study, hemodynamic improvements after valvuloplasty were manifested by a reduction in the R-MP interval. We conclude that phonocardiography may be a practical, noninvasive method of assessing the hemodynamic response to balloon aortic valvuloplasty.

Journal Article↗