Initial experience with MIDCAB grafting using the gastroepiploic artery.

BACKGROUND: Minimally invasive direct coronary artery bypass grafting with the gastroepiploic artery can be used in primary operations and reoperations to revascularize the inferior or anterior surface of the heart. METHODS: Patients who had symptomatic coronary artery disease limited to a single coronary distribution were selected. Coronary targets were grafted with the pedicled gastroepiploic artery through a small midline epigastric incision. Patients were followed with scheduled outpatient clinic visits, Doppler examination, and selective recatheterization. RESULTS: Between May 1995 and November 1997, 74 patients underwent gastroepiploic artery minimally invasive direct coronary artery bypass grafting; 33 (45%) had a primary operation and 41 (55%), a reoperation. Grafting was performed to the distal right coronary artery (n = 38), the posterior descending artery (n = 28), or the distal left anterior descending coronary artery (n = 8). There were six deaths (8%) within 30 days after operation. Twenty patients (28%) underwent recatheterization; there were two graft occlusions, two graft stenoses, and five anastomotic stenoses. Of 60 patients seen 2 or more weeks after operation, 53 (88%) had resolution of anginal symptoms at a mean follow-up of 10.9 months (range, 0 to 30 months). CONCLUSIONS: Inferior minimally invasive direct coronary artery bypass grafting with the gastroepiploic artery avoids the risks of repeat sternotomy, aortic manipulation, and cardiopulmonary bypass. Patency rates, however, were lower than expected, and there is significant morbidity and mortality associated with high-risk patients undergoing the procedure. Continued follow-up is essential to evaluate long-term graft patency and patient survival.

Assessing the impact of cerebral injury after cardiac surgery: will determining the mechanism reduce this injury?

BACKGROUND: Central nervous system dysfunction continues to produce significant morbidity and associated mortality in patients undergoing cardiac surgery. Using a closed-chest canine cardiopulmonary bypass model, dogs underwent 2 h of hypothermic circulatory arrest (HCA) at 18 degrees C, followed by resuscitation and recovery for 3 days. Animals were assessed functionally by a species-specific behavioral scale, histologically for patterns of selective neuronal necrosis, biochemically by analysis of microdialysis effluent, and by receptor autoradiography for N-methyl-D-aspartate (NMDA) glutamate receptor subtype expression. RESULTS: Using a selective NMDA (glutamate) receptor antagonist (MK801) and an AMPA antagonist (NBQX), glutamate excitotoxicity in the development of HCA-induced brain injury was documented and validated. A microdialysis technique was employed to evaluate the role of nitric oxide (NO) in neuronal cell death. Arginine plus oxygen is converted to NO plus citrulline (CIT) by the action of NO synthase (nNOS). CIT recovery in the cerebrospinal fluid and from canine cortical homogenates increased during HCA and reperfusion. These studies demonstrated that neurotoxicity after HCA involves a significant and early induction of nNOS expression, and neuronal processes leading to widespread augmentation of NO production in the brain. To further investigate the production of excitatory amino acids in the brain, we hypothesized the following scenario: HCA--> increased glutamate, increased aspartate, increased glycine--> increased intracellular Ca2+--> increased NO + CIT. Using the same animal preparation, we demonstrated that HCA caused increased intracerebral glutamate and aspartate that persists up to 20 h post-HCA. HCA also resulted in CIT (NO) production, causing a continued and delayed neurologic injury. Confirmatory evidence of the role of NO was demonstrated by a further experiment using a specific nNOS inhibitor, 7-nitroindazole. Animals underwent 2 h of HCA, and then were evaluated both physiologically and for NO production. 7-Nitroindazole reduced CIT (NO) production by 58.4 +/- 28.3%. In addition, dogs treated with this drug had superior neurologic function compared with untreated HCA controls. CONCLUSIONS: These experiments have documented the role of glutamate excitotoxicity in neurologic injury and have implicated NO as a significant neurotoxin causing necrosis and apoptosis. Continued research into the pathophysiologic mechanisms involved in cerebral injury will eventually yield a safe and reliable neuroprotectant strategy. Specific interventional agents will include glutamate receptor antagonists and specific neuronal NO synthase inhibitors.

Early experience with minimally invasive direct coronary artery bypass grafting with the internal thoracic artery.

OBJECTIVE: Minimally invasive direct coronary artery bypass is performed under direct vision without sternotomy or cardiopulmonary bypass. The technique can be used in both primary and reoperative cases by employing the internal thoracic artery to perform arterial revascularization of the anterior surface of the heart. METHODS: Patients were selected who had significant coronary artery disease limited to 1 or 2 coronary distributions on the anterior surface of the heart. Coronary target vessels were grafted with the internal thoracic artery through a small anterior thoracotomy. After partial heparinization the anastomosis was facilitated by local coronary occlusion and handheld stabilization. RESULTS: Between August 1994 and July 1997, 162 patients underwent minimally invasive direct coronary artery bypass grafting with the internal thoracic artery. The left and right internal thoracic arteries were used for grafting of the left anterior descending artery in 142 patients (88%), the proximal right coronary artery in 7 patients (4%), existing saphenous vein grafts in 5 patients (3%), and diagonal branches in 2 patients (1%). Sequential grafting with the left internal thoracic artery was performed in 2 patients (1%) and bilateral internal thoracic artery grafting was performed in 4 patients (3%). Eight patients (4.9%) died within 30 days after the operation, 3 of cardiac causes. Seven additional patients died during the follow-up period. Nine patients (5.6%) required reintervention for graft stenosis or occlusion during follow-up. Of 141 patients seen 2 or more weeks after the operation, 135 (96%) had resolution of their anginal symptoms at a mean follow-up of 12 months (range 0-31 months). CONCLUSIONS: Anterior minimally invasive direct coronary artery bypass grafting with the internal thoracic artery avoids the risks of repeated sternotomy, aortic manipulation, and cardiopulmonary bypass. There was a low rate of reintervention, and patients had excellent resolution of anginal symptoms. Postoperative length of stay was comparatively short, and continued follow-up will be essential to evaluate long-term graft patency and patient survival.

Conservative management of late rejection after heart transplantation: a 10-year analysis.

OBJECTIVE: Immunosuppressive regimens for rejection after heart transplantation have been modified to reduce infectious complications without diminishing rejection treatment efficacy. A review of a single institutional series was performed to evaluate the influence of conservative management of grade 2 rejection on long-term outcomes after heart transplantation. METHODS: Before 1990, patients with late (>3 months after transplant) grade 2 rejection were treated with supplemental immunosuppressive drugs. Beginning in 1990, patients with late grade 2 rejection were treated conservatively by maintaining the current immunosuppressive regimen without additional therapy. The groups were compared for survival, incidence of subsequent rejection, and incidence of subsequent infection. RESULTS: One hundred twelve patients had one or more episodes of isolated, late grade 2 rejection; 39 (35%) were treated with supplemental immunosuppression (treated group) and 73 (65%) received no additional therapy (nontreated group). The mean time from transplantation to the first episode of isolated grade 2 rejection was 15.6 months in the treated group and 17.8 months in the nontreated group. Graft survival at 5 and 10 years was 69% and 51 %, respectively, in the treated group and 67% and 41 %, respectively, in the nontreated group (p = 0.77). The rates for overall subsequent rejection were 0.031 episodes/patient-month in the treated group and 0.029 episodes/patient-month in the nontreated group (p = 0.64). The rates for early rejection within 6 months of initial grade 2 rejection were 0.044 episodes/patient-month in the treated group and 0.035 episodes/patient-month in the nontreated group (p = 0.56). The rates for overall subsequent infection were 0.018 episodes/patient-month in the treated group and 0.012 episodes/patient-month in the nontreated group (p = 0.05). The rates for early infection within 6 months of initial grade 2 rejection were 0.070 episodes/patient-month in the treated group and 0.032 episodes/patient-month in the nontreated group (p = 0.04). Group comparisons demonstrated a significantly lower incidence of infection in the nontreated group. CONCLUSIONS: Conservative management of late grade 2 rejection neither adversely affects survival nor increases the incidence of subsequent short-term or long-term rejection. This approach lowers the early and late incidence of infection after rejection and may reduce other complications from aggressive supplemental immunosuppression.

Reoperative MIDCAB grafting: 3-year clinical experience.

OBJECTIVE: Minimally invasive direct coronary artery bypass (MIDCAB) is performed under direct vision without sternotomy or cardiopulmonary bypass. The technique is used in reoperative patients through various incisions to revascularize one or two areas of the heart. The internal mammary artery, gastroepiploic artery, radial artery, or saphenous vein are used as graft conduits. METHODS: Anterior coronary targets are grafted with the internal mammary artery via a small anterior thoracotomy. Inferior coronary targets are grafted with the gastroepiploic artery via a small midline epigastric incision. Lateral coronary targets are grafted with radial artery or saphenous vein via a posterior thoracotomy. After partial heparinization, the anastomosis is facilitated by local coronary occlusion and stabilization. Graft follow-up consists of outpatient Doppler examination and selective recatheterization. RESULTS: Between January 1994 and August 1997, 81 patients underwent reoperative MIDCAB grafting. Twenty-one patients (25.9%) had internal mammary grafting, 39 (48.2%) had gastroepiploic grafting, and 21 (25.9%) had lateral grafting with radial artery or saphenous vein. There were nine early deaths (four cardiac, five non-cardiac), five late deaths (three cardiac, two non-cardiac), and nine myocardial infarctions in remaining patients. Sixteen patients underwent recatheterization; there were one graft occlusion, two graft stenoses, and eight anastomotic stenoses. Mean postoperative length of stay was 3.8 days. Ninety percent (55/61) of patients are free of symptoms at a mean follow-up of 7.8 months (range 0-39). CONCLUSIONS: Reoperative MIDCAB grafting avoids the risks of resternotomy, aortic manipulation, and cardiopulmonary bypass. The techniques yield an early patency rate of 94%, which includes eight patients who had postoperative catheter-based interventions. Reoperative MIDCAB grafting had lower rates of supraventricular arrhythmia and transfusion when compared with conventional coronary artery bypass grafting, but did not offer an advantage for mortality, stroke or myocardial infarction. This 3-year experience suggests that while reoperative MIDCAB grafting can effectively revascularize focal areas of the heart, patients should be carefully selected to minimize operative risk.

Peripheral vascular complications after intracoronary stent placement: prevention by use of a pneumatic vascular compression device.

Peripheral vascular complications are a significant source of morbidity after coronary artery stent implantation. The goal of this study was to assess the incidence, risk factors, and management of vascular complications after stent placement. The study population consisted of 101 consecutive patients who underwent stent placement for either elective or bailout indications. All patients received a standardized anticoagulation regimen of aspirin, dipyridamole, low molecular weight dextran, heparin, and warfarin. Peripheral vascular access sites were examined daily until hospital discharge. Vascular complications occurred in 16 of 101 (16%) patients, including femoral artery pseudoaneurysm (n = 11), hematoma requiring transfusion or surgery (n = 4), and arteriovenous fistula (n = 1). Intervention was required in 14 of 16 (88%) patients with complications. These included transfusion (n = 7), ultrasound-guided compression (n = 8), and/or vascular surgery (n = 7). Length of hospital stay was prolonged in patients with complications (14 +/- 9 vs. 8 +/- 5 d, P < 0.001). The development of peripheral vascular complications did not correlate with clinical or procedural variables such as age, cardiovascular risk factors, arterial sheath size, or elective vs. bailout indication. After the introduction of a pneumatic vascular compression device (FEMOSTOP, C.A. Bard, Billerica, MA), a significant reduction in vascular complications was observed. Complications occurred in only 1 of 41 (2.4%) patients in whom the compression device was used in contrast to 13 of 58 (22.4%) patients compressed manually (P < 0.01). Thus peripheral vascular complications are frequent after coronary artery stent placement and are associated with serious morbidity and prolongation of hospital stay. These complications are significantly reduced by the use of a pneumatic vascular compression device despite intensive systemic anticoagulation.

Comparison of coronary angiographic findings during the first six hours of non-Q-wave and Q-wave myocardial infarction.

The angiographic features of non-Q-wave acute myocardial infarction (AMI) soon after symptom onset have not been previously reported. Accordingly, this study reviewed the coronary angiographic findings of 86 patients with AMI studied within 6 hours of symptom onset: 58 had Q-wave and 28 had non-Q-wave AMI. Patients with Q-wave and non-Q-wave AMI were comparable in terms of clinical characteristics, frequency of 1-vessel disease, and infarct-related artery location. Thrombus was observed in 49 patients (84%) with Q-wave AMI versus 12 (43%) with non-Q-wave AMI (p = 0.0002). Whereas complete occlusion of the infarct-related artery was present in 53 patients (91%) with Q-wave AMI, total coronary occlusion was present in only 11 (39%) with non-Q-wave AMI (p = 0.0001). Collaterals to occluded infarct arteries were seen in 10 patients (19%) with Q-wave AMI versus 5 (45%) with non-Q-wave AMI (p = 0.06). Residual perfusion of the infarct artery by either anterograde or collateral flow was typical of patients with non-Q-wave AMI (22 of 28, 79%) but was uncommon in those with Q-wave AMI (15 of 58, 26%) (p = 0.0001). Thus, coronary angiography performed within 6 hours of symptom onset demonstrates important differences between Q-wave and non-Q-wave AMI. Non-Q-wave AMI is characterized by partial perfusion of the infarct-related artery by either anterograde or collateral flow, and a lower incidence of thrombus than Q-wave AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Advanced radiofrequency catheter ablation in canine myocardium.

Current radiofrequency (RF) ablation technology is limited by small lesion size. To enhance the size of RF-induced left ventricular (LV) endocardial lesions, we evaluated the effects of an enlarged distal electrode tip and increased RF power on lesion volume. Steerable electrode catheters with distal electrode tips of 4 to 12 mm were studied in anesthetized dogs at power settings of 20 to 100 W. Temperature was continuously monitored from a thermistor located at the tip of the catheter. RF energy (500 kHz, unmodulated) was applied between the tip of the catheter and a large skin electrode at four separate LV sites in each animal. Hearts were excised, frozen, sectioned, and stained with nitroblue tetrazolium. Lesion area was planimetered and volume was calculated. Lesion volume increased with increasing electrode size and delivered power. However, a rise in impedance limited maximal lesion size at higher power with each electrode. Maximal lesion size with an 8 mm tip was approximately twice the size of the maximal lesion with a 4 mm tip (914 +/- 362 mm3 vs 460 +/- 150 mm3, p < 0.01). Minimal lesions were seen with large tip electrodes at power < 40 W because of low tip temperature (< 55 degrees C). Average tip temperature correlated with measured lesion volume (r = 0.7). Ventricular fibrillation occurred in approximately one half of the animals studied, and was associated with larger lesion volume (p < 0.01). Catheter ablation of ventricular tachycardia may be enhanced by this technology.

Microwave thermal balloon angioplasty in the atherosclerotic rabbit.

We evaluated the angiographic and histologic response of the coronary vessels of the atherosclerotic rabbit to microwave thermal balloon angioplasty. Sixteen rabbits with atherosclerosis of the external iliac arteries following a high fat diet and endothelial denudation were treated with either CBA or MBA. Four weeks following angioplasty angiography was repeated, and following the death of the animals, the vessels treated were excised for histologic evaluation. In vessels with MBA with peak temperatures of 85 degrees C there was an increase in luminal diameter immediately postangioplasty, from 1.66 +/- 0.32 mm to 2.54 +/- 0.23 mm (p < 0.05). The diameter at 4 weeks (2.29 +/- 0.74 mm) remained increased compared with the preangioplasty diameter (p < 0.05). With microwave angioplasty at 70 degrees C there was an increase in luminal diameter, from 1.92 +/- 0.37 mm to 2.40 +/- 0.22 mm (p < 0.05) immediately postangioplasty. This increase in diameter was not sustained at 4 weeks (1.86 +/- 0.28 mm). In the vessels treated with CBA there was no significant increase in diameter noted either immediately postangioplasty or at 4 weeks postangioplasty. In the thermally treated vessels, histologic evaluation revealed a loss of lipid-laden cells; it also revealed the formation of a concentric hypocellular fibrotic layer. Microwave thermal balloon angioplasty at 85 degrees C results in enhancement of the immediate and delayed response to angioplasty. Modification of the proliferative response to angioplasty may be accomplished with this modality.

Microwave thermal balloon angioplasty in the normal rabbit.

The feasibility of utilizing microwave energy for thermal angioplasty was evaluated in 28 normal New Zealand white rabbits. Angioplasty catheters were inserted via bilateral femoral arteriotomy and balloon angioplasty was performed on the external iliac arteries. There were three variables in the microwave angioplasty procedure: peak temperature, energy duration, and peak balloon pressure. At 1 week after the angioplasty, animals were put to death and the iliac arteries were removed after perfusion fixation. Histologic analysis was performed. Injuries to the medial and intimal proliferation were evaluated using an index based on the circumferential extent and depth of abnormality. There was no relationship noted between intimal proliferation or medial injury and energy duration of peak balloon pressure. There was a direct relationship between peak temperature and medial injury. Furthermore, there was an inverse relationship between medial injury and intimal proliferation. The axial extent of change induced by microwave energy was 1.6 cm. Microwave thermal energy delivery through a balloon angioplasty catheter is feasible and can be performed conveniently.

Fibrinolytic activity after vessel wall injury.

The goal of this study was to assess fibrinolytic activity after vessel wall injury and to correlate changes in fibrinolytic activity with angiographic and histologic findings. Accordingly, in 18 atherosclerotic rabbits, vessel wall injury was produced by means of iliac artery balloon angioplasty (the injury group), whereas 8 atherosclerotic rabbits served as a control group. In all rabbits from the injury group, deep vessel wall injury was documented by either angiography or histologic study. Plasminogen activator inhibitor-1 activity in plasma increased significantly, from 21.79 +/- 1.29 arbitrary units/ml (AU/ml) at baseline study to 32.05 +/- 1.47 AU/ml at 6 h after vessel wall injury (p less than 0.01), whereas activity remained unchanged throughout the 24-h period in the control group. Plasma levels of tissue plasminogen activator activity were similar in both groups. Intravascular thrombus was found in five of six additional rabbits 6 h after vessel wall injury, that is, at the time of impaired fibrinolytic activity, whereas no thrombus was found in the control group (p less than 0.05). It is concluded that deep vessel wall injury is associated with reduced fibrinolytic activity. In addition to other procoagulant factors, elevated plasminogen activator inhibitor-1 activity may lead to intravascular thrombosis and impaired resolution of thrombus.

Does antiplatelet therapy enhance myocardial salvage after coronary reperfusion?

The aim of this study was to test the hypothesis that either the cyclooxygenase inhibitor aspirin or the thromboxane A2 receptor antagonist sulotroban exerts a direct myocardial effect that enhances myocardial salvage afforded by reperfusion. Accordingly, 21 anesthetized dogs underwent suture occlusion of the left anterior descending coronary artery. At 2.5 h after occlusion, all dogs received intravenous streptokinase (20,000 U/kg body weight over 30 min) and were randomized to the following groups: group I (n = 7) received no additional treatment, group II (n = 7) received aspirin (5 mg/kg intravenously) and group III (n = 7) received sulotroban (10 mg/kg followed by 10 mg/kg per h intravenously). At 3 h after occlusion, the dogs underwent coronary reperfusion for the next 3 h. Myocardial infarct size as a percent of the hypoperfused zone was similar among dogs in group I (42 +/- 8%), group II (41 +/- 10%) and group III (45 +/- 11%). The incidence and the extent of myocardial hemorrhage were similar in all three study groups. Infarct size as a percent of the hypoperfused zone was significantly smaller in dogs without hemorrhage irrespective of treatment (35 +/- 9% versus 63 +/- 5%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Lisinopril for severe congestive heart failure.

Lisinopril, a new converting enzyme inhibitor, was studied hemodynamically in 55 patients. The response to 2.5-, 5- and 10-mg doses showed significant increases in cardiac index and significant reductions in pulmonary artery wedge, right atrial, pulmonary arterial and systemic arterial pressures, as well as in systemic vascular resistance. Significant changes in most parameters were present at 24 hours. A dose-response relation for most parameters was noted. Over a 3-month period, 47 patients were followed up, with improvement in functional capacity and symptomatic status. Metabolic parameters did not change over time, although 26% showed evidence of reversible renal dysfunction. Only 3 patients (6.4%) required discontinuation because of adverse effects. A subgroup of patients reassessed at 3 months demonstrated maintenance of hemodynamic effects. The present study demonstrates that (1) the hemodynamic effects of lisinopril are of relatively long duration; (2) within certain limits, a dose-response relation can be defined; and (3) the drug has an acceptable long-term tolerability profile.

Modulation of hemodynamic effects with a converting enzyme inhibitor: acute hemodynamic dose-response relationship of a new angiotensin converting enzyme inhibitor, lisinopril, with observations on long-term clinical, functional, and biochemical responses.

The hemodynamic effects of varying oral doses of the long-acting converting enzyme inhibitor lisinopril were studied in an acute, single-blind, parallel fashion in 55 patients with moderate to severe congestive heart failure. Doses of 2.5, 5.0, and 10 mg produced a significant increase in cardiac index and significant reductions in pulmonary capillary wedge, right atrial, pulmonary arterial, and systemic arterial pressures and systemic vascular resistance. The changes were present up to 24 hours after dosing for most parameters. There was a clear-cut dose-response relationship observed. Forty-seven patients were followed over a 3-month period, during which functional status and exercise tolerance improved. Although 26% showed some evidence of renal dysfunction with lisinopril, these changes could be normalized by decreasing either the lisinopril or the diuretic dose. These data demonstrate that the hemodynamic changes with the long-acting converting enzyme inhibitor lisinopril can be modulated with dose adjustment in patients with congestive heart failure. They also suggest that renal function changes may be normalized by adjustment of either the dose of lisinopril or the diuretic dose.

Hemodynamics of human arterial stenoses.

We assessed the hemodynamic and geometric changes in compliant, human arterial stenoses in response to manipulation of vascular tone, perfusion pressure and distal resistance. Coronary and popliteal arteries were harvested from human cadavers shortly after death. Following incubation for several hours to permit recovery of physiologic energy stores and ion gradients, the vessels were attached to a perfusion apparatus and perfusion pressure (PP), distal pressure (DP), and flow (F) were recorded as perfusion pressure and distal resistance (DR) were varied. The experiments were then repeated in the presence of a vasoconstrictor (100 mM KCl). Orthogonal arteriograms were performed at maximums of vasoconstriction and vasodilation. Stenotic resistance (SR) was calculated as (PP-DP)F. Minimum cross-sectional area was determined by computer assisted analysis of the arteriograms. Stenosed vessels with normal wall segments at the stenosis responded to vasoconstriction with a large stenotic resistance increase (111 +/- 15%; P less than 0.05) and a flow decrease averaging 39.3 +/- 6.2% (P less than 0.05). In addition, decreased perfusion pressure also increased stenotic resistance significantly (P less than 0.05). Stenotic resistance changes were of sufficient magnitude to be both statistically significant and clinically important. These results confirm the existence of dynamic arterial stenoses in humans and further support the assertion that dynamic stenotic severity changes elicited by manipulation of proximal and distal vascular tone and pressure are of sufficient magnitude to create acute ischemia. This information may apply to clinical situations in which compliant stenoses and acute ischemia coexist.

Thromboxane A2 in acute myocardial infarction.

We evaluated the presence of thromboxane B2, the stable metabolite of thromboxane A2, early in the course of acute myocardial infarction (AMI) in both animal and patient studies. In an open-chest model, the left anterior descending artery (LAD) was isolated and the great cardiac vein was cannulated in nine dogs. Following occlusion of the LAD, there was an increase in thromboxane B2 concentration from 0.77 +/- 0.0093 to 1.79 +/- 0.46 pmol/ml (p less than 0.05) and 1.96 +/- 0.48 pmol/ml (p less than 0.05) at 1 and 5 minutes, respectively, following coronary occlusion. At 30 and 60 minutes after occlusion there was no significant increase compared to the baseline. In 17 patients with AMI the mean thromboxane B2 concentration was 0.96 +/- 0.13 pmol/ml at 4.88 +/- 0.40 hours after the onset of chest pain. In 12 patients with sequential samples before and after restoration of patency of the occluded vessel, the initial concentration was 0.71 +/- 0.058 pmol/ml. At 5 minutes after restoration of patency thromboxane B2 concentration was 1.1 +/- 0.17 pmol/ml (p = 0.05). One hour later a return to baseline was noted (0.82 +/- 0.75 pmol/ml). Two patients with the highest thromboxane B2 concentrations (2.0 and 2.6 pmol/ml) were unable to have successful recanalization. We conclude that generation of thromboxane A2 occurs during the early stages of AMI and may be an important pathophysiologic phenomenon in AMI.

Intracoronary thrombolysis in acute myocardial infarction: clinical course following successful myocardial reperfusion.

We reviewed the clinical course of 73 patients who had attempted intracoronary thrombolysis, with emphasis on follow-up. Fifty-nine patients (81%) had coronary reflow sufficient to control pain and injury current: 52 received thrombolysis alone and seven had thrombolysis combined with acute coronary angioplasty. Recurrent ischemic events in hospital were frequent and occurred in 17 patients (29%). These included silent reocclusion (four patients), recurrent angina (eight patients), and recurrent infarction in the same myocardial zone (five patients). Late ischemic events occurred in 11 patients (19%) and included silent reocclusion (two patients) and angina (nine patients). Although acute coronary angioplasty resulted in a high rate of successful myocardial reperfusion, long-term vessel patency was infrequent. The results of coronary bypass surgery, performed in hospital for severe residual coronary stenosis and angina and later for recurrent angina, were uniformly good. At follow-up of 6 to 36 months (mean 18.5 +/- 8.1), total mortality was five patients (8%). Only 16 reperfused patients (27%) were alive and well without recurrent ischemia or interventions. We conclude that reopening an acutely occluded coronary artery by thrombolysis and/or angioplasty can be performed in the majority of patients but must be regarded as initial therapy in view of the high incidence of recurrent ischemic events. Reperfused patients with stable myocardial blood supply post infarction have low long-term mortality.

Potentiation of coronary vascular platelet adhesion by atrial pacing in the presence of arterial stenosis in dogs.

The effect of atrial pacing on coronary hemodynamics and platelet adhesion was evaluated in 13 dogs. In all 13 dogs, a snare was placed around the circumflex artery and tightened so that distal coronary artery pressure decreased to 60 to 70 mm Hg. In 10 dogs, atrial pacing was instituted at twice the heart rate at rest for 10 minutes. In three dogs, observation was continued for 10 minutes without pacing. In the 10 dogs undergoing pacing, heart rate increased from 90.5 +/- 32.6 to 173.5 +/- 45.8 beats/min. Aortic pressure was unchanged. Distal coronary artery pressure decreased from 70.8 +/- 7.8 to 53.2 +/- 10.0 mm Hg (p less than 0.05) and the pressure gradient across the stenosis increased from 47.6 +/- 12.7 to 61.2 +/- 9.1 mm Hg (p less than 0.05). Stenotic resistance increased from 2.5 +/- 0.8 to 3.6 +/- 2.4 mm Hg/ml X min-1, but coronary flow was unchanged. In all three control dogs, there was no change in coronary dynamics for the 10 minute period. In 8 of the 10 dogs that underwent pacing, platelet deposition was observed at the site of coronary stenosis. In contrast, in the three control dogs there was no platelet deposition. Atrial pacing in the presence of coronary stenosis appears to alter coronary hemodynamics such that there are activation and deposition of platelets at the site of stenosis. This platelet deposition may be transient or could become the nidus for subsequent platelet-related events in the coronary vessel.