Transcatheter electrical shock ablation of ventricular tachycardia.

Transcatheter shock ablation of ventricular tachycardia was attempted in seven patients who had drug-resistant ventricular tachycardia and in one patient in whom ventricular tachycardia was electrophysiologically induced during therapy with multiple antiarrhythmic drugs. Seven patients had previous myocardial infarction and five of them were high risk candidates for surgical therapy. One patient without organic heart disease had repetitive ventricular tachycardia manifesting two different patterns of left bundle branch block. After endocardial mapping, synchronized unipolar 250 to 300 J shocks (one to six) were delivered between the pole recording the earliest endocardial activity during ventricular tachycardia (40 to 200 ms before the onset of the QRS complex) and a body surface electrode. Immediate complications included severe but reversible cardiogenic shock (one patient), nonclinical ventricular tachycardia (two patients, requiring cardioversion in one), transient atrioventricular and intraventricular conduction disturbances (three patients) and permanent left bundle branch block (one patient). A late complication in one patient, left heart failure, occurred 3 days after delivery of five intracardiac shocks. In two patients, left ventricular ejection fraction markedly decreased and in one of them new ventricular contraction abnormalities appeared. Clinical ventricular tachycardia did not recur in five of the seven post-myocardial infarction patients after 7 to 17 months, and it was not inducible in the four patients undergoing late electrophysiologic study. In the patient with idiopathic ventricular tachycardia, one of the configurational types of ventricular tachycardia recurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Intermittent poppet dislodgment in a Braunwald-Cutter prosthesis: noninvasive diagnosis and successful surgical treatment.

A 65 year old patient had his mitral and aortic valves replaced with two Braunwald-Cutter prostheses in 1973. Seven years later, he presented with intermittent aortic insufficiency demonstrated by echocardiography, fluoroscopy and angiography. At emergency surgery, the occluders (poppets) of both prostheses were found within the left ventricular cavity. The valves were excised and replaced with Björk-Shiley prostheses and the patient recovered. Aortic occluder escape is rare and usually fatal. Mitral occluder escape of the Braunwald-Cutter prosthesis has not been described previously.

Early intervention in acute myocardial infarction: significance for myocardial salvage of immediate intravenous streptokinase therapy followed by coronary angioplasty.

Sixteen patients with acute myocardial infarction underwent treatment with streptokinase up to 3 hours after the onset of chest pain. Nine patients (group I) received streptokinase within 1 hour of the onset of pain, and seven patients (group II) received it within 2 to 3 hours. All underwent multigated radionuclide ventriculography after streptokinase therapy and 1 week later. Percutaneous transluminal coronary angioplasty of the infarct artery was performed within 24 hours in all patients. An effort-limited treadmill stress test was performed before discharge. There was no mortality or serious complication. Mean peak total creatine kinase was 521 +/- 289 mU/ml in group I, and 1,614 +/- 709 mU/ml in group II (p less than 0.05). The mean initial left ventricular ejection fraction was 47 +/- 11% in group I and 37 +/- 10% in group II. After early angioplasty (within 24 hours) and at 1 week recovery, left ventricular ejection fraction increased to 53 +/- 9% in group I (p less than 0.05) and to 40 +/- 7% in group II (p = NS). Seven of the nine patients in group I had normal radionuclide ventriculograms at discharge compared with none of the seven patients in group II. Thrombolytic therapy administered less than 1 hour after the onset of symptoms of acute myocardial infarction followed by angioplasty of the infarct artery results in preservation of left ventricular function, whereas therapy given after 2 hours has only a limited effect.

Myocardial risk area defined by technetium-99m sestamibi imaging during percutaneous transluminal coronary angioplasty: comparison with coronary angiography.

OBJECTIVES: The purpose of this study was to compare the assessment of myocardial area at risk in patients with coronary artery stenosis by coronary angiography and quantitative myocardial perfusion imaging with technetium-99m sestamibi. BACKGROUND: Decisions concerning patient management frequently rely on semiquantitative angiographic estimation of the myocardial area at risk, although this approach has not been well validated. Technetium-99m sestamibi is a perfusion imaging agent with little redistribution after initial myocardial uptake. This characteristic allows for injection during angioplasty and later imaging for visualization and quantitation of the nonperfused area at risk. METHODS: Thirty-nine patients referred for coronary angioplasty were studied. Technetium-99m sestamibi was injected intravenously during angioplasty balloon inflation. Planar (33 patients) or tomographic (6 patients) imaging was performed after completion of angioplasty. Imaging was repeated 24 to 48 h later. Myocardial risk area (perfusion defect on angioplasty image) was quantified as an integral using circumferential count distribution profiles and normal reference. Angiographic risk area was assessed using five scoring methods. RESULTS: The scintigraphic risk area was 14 +/- 15 on planar images and 39 +/- 16 on tomography. Scintigraphic risk area of patients with infarction was larger than in patients without (22 +/- 17 versus 7 +/- 8, p = 0.003). The left anterior descending coronary artery had a larger mean risk area than other vessels (22 +/- 15 versus 7 +/- 11, p = 0.002). The presence of angiographic collateral channels was associated with smaller risk areas. Angiographic risk scores correlated only moderately with the technetium-99m sestamibi risk area (r = 0.54 to 0.65), with considerable spread of data. CONCLUSIONS: Area at risk estimated from coronary angiography does not correlate well with that from quantitative myocardial perfusion imaging with technetium-99m sestamibi. These findings emphasize that the functional significance of coronary artery disease is not predicted by coronary anatomy alone.

Repeat infusion of recombinant tissue-type plasminogen activator in patients with acute myocardial infarction and early recurrent myocardial ischemia.

When conventional treatment of patients with early clinical reinfarction after thrombolytic therapy fails, mechanical revascularization may be attempted. An alternative strategy, repeat thrombolytic infusions, is reported. Fifty-two patients with acute myocardial infarction were treated with one or two additional thrombolytic infusions of recombinant tissue-type plasminogen activator (rt-PA) because of nonsustained ischemia after initial treatment with rt-PA or streptokinase. Thirty-five patients received the second infusion within 1 h of the first; 13 patients received the second infusion 1 to 72 h after the first and 4 patients received it later during their hospitalization. Bleeding complications occurred in 10 patients (19%); however, most of these were minor (no intracranial bleeding) and only 2 patients required blood transfusion. In 14 patients in whom the decrease in fibrinogen and plasminogen levels was measured after the first and second infusions, this decrease was only 25% and 63%, respectively--only slightly higher than the 22% and 53% decreases measured in 63 patients who had only one rt-PA infusion. In 44 patients (85%), the acute ischemia resolved completely within 1 h after initiation of the second infusion. In 23 patients (44%), pain and ST segment elevation did not recur and invasive coronary intervention was avoided. Thus, repeat rt-PA infusions can stabilize a substantial number of patients with acute reinfarction and, even when relief is temporary, repeat rt-PA infusions can minimize myocardial damage while patients await mechanical revascularization.

Should thrombolytic therapy be administered in the mobile intensive care unit in patients with evolving myocardial infarction? A pilot study.

The growing recognition of the importance of early thrombolysis in evolving myocardial infarction was the basis for the present study, which evaluated the effectiveness, feasibility and safety of prehospital thrombolytic therapy. In a relatively small study, 118 patients were allocated to receive either prehospital treatment with recombinant tissue-type plasminogen activator (rt-PA) in the mobile intensive care unit (group A, 74 patients) or hospital treatment (group B, 44 patients). A total of 120 mg of rt-PA was infused over a period of 6 h. All patients were fully heparinized and underwent radionuclide left ventriculography and coronary angiography during hospitalization. Although group A was treated significantly earlier than group B after onset of symptoms (94 +/- 36 versus 137 +/- 45 min, respectively; p less than 0.001), no significant differences were observed between the groups in 1) extent of myocardial necrosis, 2) global left ventricular ejection fraction at discharge, 3) patency of infarct-related artery, 4) length of hospital stay, and 5) mortality at 60 days. However, a trend to a lower incidence of congestive heart failure at hospital discharge was observed in the prehospital-treated compared with the hospital-treated group (7% versus 16%, respectively; p = NS). No major complications occurred during transportation. It is concluded that myocardial infarction can be accurately diagnosed and thrombolytic therapy initiated relatively safely during the prehospital phase by the mobile intensive care team, thus instituting a beneficial clinical trend in favor of prehospital thrombolysis.

Study of the mechanism of ultrasound angioplasty from human thrombi and bovine aorta.

Ultrasound angioplasty is a newly developed technology for percutaneous arterial recanalization. Data suggest that ultrasound is particularly effective in ablating fresh thrombi. Arterial walls were found to be resistant to ultrasound ablation. Thrombi, aortic wall segments, and hydroxyproline gelatin were studied in vitro to determine their respective ablation rates. The elasticity of the samples was determined in a force-mode apparatus. The cavitation threshold was determined in an arterial phantom apparatus. Thrombi displayed ablation rates that were > 20 times higher than those of aortic wall samples (591 +/- 82 vs 25 +/- 14 mg/s, p < 0.001). The differences in ablation rates were accompanied by significantly lower elasticities in the thrombus group compared with those in the aortic wall group (0.16 +/- 0.05 vs 312 +/- 37 g/cm2, p < 0.001). Experiments with hydroxyproline gelatin suggest a negative correlation (r = -0.90) between elasticity and ultrasound ablation. Ultrasound ablation of thrombi was evident only above the cavitation threshold. Thus, ultrasound angioplasty has the potential to induce the selective injury required for successful transluminal intervention in the treatment of thrombus-rich lesions.

Changes in hemostatic function at times of cyclic variation in occupational stress.

In this study we demonstrated, in the same healthy subjects, a significant elevation in coagulation factors VII and VIII, fibrinogen, thrombocyte count, and thrombin and adenosine diphosphate-induced platelet aggregation during a period of increased workload compared with a calm work period. These findings may add to the understanding of the mechanism that links mental stress to coronary disease.

Intravascular ultrasound characterization of thrombi of different composition.

An in vitro model was designed to test the hypothesis that thrombi of varying composition have different echogenic patterns. Thrombi were prepared in specially designed tubes, mounted on a holder that allows introduction of an intravascular ultrasound catheter rotated inside a subselective sheath. The thrombi were made by the addition of thrombin to whole blood, platelet-rich plasma, and to mixtures of whole blood and platelet-rich plasma with increasing concentration of whole blood relative to the volume of the mixture in the following ratios: 1:5, 2:5, 3:5 and 4:5. Sixty-six thrombi prepared from 11 blood samples of healthy subjects were studied and compared with control tubes filled with saline solution. Platelet-rich thrombi showed low echogenicity similar to saline solution. Whole blood thrombi appeared uniformly "speckled." Mixtures of whole blood and platelet-rich plasma showed a gradual increase in echogenicity with an increasing amount of whole blood in the mixture. Quantitative videodensitometry compared the gray scale intensity of each image relative to background saline. The mean value of echogenicity of platelet-rich thrombi was 0.9 +/- 1.2, and the mean value of whole blood thrombi was 13 +/- 5.3. Platelet-rich thrombi are echo-lucent, and the main echogenic reflectance of thrombi originates from red blood cells. The ultrasound intensity is in linear relation to the amount of red blood cells in the thrombus.

Correlation of baseline plasminogen activator inhibitor activity with patency of the infarct artery after thrombolytic therapy in acute myocardial infarction.

Increased levels of plasminogen activator inhibitor (PAI) have recently been described in patients with acute myocardial infarction (AMI). To correlate PAI levels to patency of infarct arteries after thrombolytic therapy with recombinant tissue-type plasminogen activator (rt-PA), 125 consecutive patients with AMI were examined. Blood levels of fibrinogen, plasminogen, tissue plasminogen activator (t-PA) and PAI were measured before treatment initiation, 10 minutes after completion of rt-PA infusion and 24 and 48 hours after treatment. Coronary angiography, performed in all patients 72 hours after beginning rt-PA infusion, revealed patent infarct arteries in 97 patients and occluded infarct arteries in 28 patients. Pretreatment levels of PAI were significantly higher in patients with occluded infarct arteries (18.0 +/- 11.5 vs 10.5 +/- 9.3 IU/ml, p less than 0.01). Conceivably, higher levels of PAI may interfere with the natural thrombolytic process and make pharmacologic thrombolytic intervention less effective.

Randomized controlled trial of late in-hospital angiography and angioplasty versus conservative management after treatment with recombinant tissue-type plasminogen activator in acute myocardial infarction.

Although both the European Cooperative Study Group and the Thrombolysis in Myocardial Infarction IIB trial indicated that angiography and angioplasty as routine measures after thrombolytic treatment do not improve clinical outcome in patients with acute myocardial infarction, the potential benefit of angioplasty may have been negated by the fact that the procedure was performed too soon (less than 32 hours) after admission. A similar study was designed in which delayed invasive treatment was compared with conservative treatment in 201 patients with acute myocardial infarction given recombinant tissue-type plasminogen activator. The 97 patients randomized to the invasive group underwent routine coronary angiography and angioplasty 5 +/- 2 days after thrombolytic therapy, whereas the 104 patients randomized to the conservative group underwent angiography only for recurrent postinfarction angina or exercise-induced ischemia. Baseline characteristics of both groups were similar. In the invasive group, 92 patients underwent angiography, 49 angioplasty and 11 coronary artery bypass surgery. In the conservative group, 40 patients experienced early ischemia, 39 underwent angiography, 20 angioplasty and 4 coronary artery bypass surgery. Reinfarction rate and preservation of left ventricular function at discharge or 8 weeks after discharge did not differ in the 2 groups. Total mortality after a mean follow-up of 10 months was 8 of 97 in the invasive and 4 of 104 in the conservative groups (p = 0.15). However, if only patients who died after the timing of the scheduled protocol catheterization in the invasive arm were included, mortality was 5 of 94 and 0 of 100 in the invasive and conservative treatment groups, respectively (p = 0.02). (ABSTRACT TRUNCATED AT 250 WORDS)

Improved survival but not left ventricular function with early and prehospital treatment with tissue plasminogen activator in acute myocardial infarction.

One hundred ninety patients with acute myocardial infarction (AMI) were treated with recombinant tissue-type plasminogen activator (rt-PA) 2.0 +/- 0.8 hours after the onset of symptoms. Eighty-seven patients were enrolled via mobile intensive care units and 103 through the emergency ward. Patients who were enrolled via the mobile intensive care units were randomized to immediate, prehospital treatment initiation, or to delayed, in-hospital treatment initiation. All 190 patients except 2 underwent delayed coronary angiography and, when indicated, angioplasty at 72 hours after enrollment. Patients treated within 2 hours and those treated 2 to 4 hours after symptom onset had similar preservation of left ventricular function, and similar prevalence of congestive heart failure at discharge. Patients treated within 2 hours of symptom onset had significantly lower short- (0.0 vs 6.3%, p = 0.01) and long-term (1.0 vs 9.5%, p = 0.03) mortality. Prehospital initiation of rt-PA appeared to be safe and feasible and resulted in a 40-minute decrease in the time from symptom onset to treatment initiation.

Serum lipids and restenosis after successful percutaneous transluminal coronary angioplasty. Ichilov Magnesium Study Group.

The effects of plasma lipids on the clinical and angiographic parameters of 134 patients, in whom coronary angioplasty was performed in 157 vessels, were prospectively examined. During a 6-month follow-up, restenosis was detected angiographically in 39 patients (29%; 45 vessels). None of the clinical, biochemical, or angiographic variables examined was predictive of stenosis and the tendency of a vessel to restenose was not patient-dependent but rather lesion-related. However, restenosis developed in 31 of 102 vessels (30%) in patients with high-density lipoprotein (HDL) cholesterol < or = 40 mg/dl, compared with restenosis in 10 of 55 vessels (19%) in patients with HDL cholesterol > 40 mg/dl (p = 0.092). No significant differences were observed when restenosis rates were compared in patients with total cholesterol levels > 250 mg/dl or < 250 mg/dl; no differences were seen in low-density lipoprotein (LDL) cholesterol levels when comparing patients with > 160 mg/dl and < 160 mg/dl. In 117 patients (132 vessels), complete serial blood specimens were obtained until the concluding angiography at 6 months. During follow-up, both groups (those with and without restenosis) had almost similar findings. Triglycerides decreased equally in both groups, and total cholesterol increased mildly in those who had restenosis; HDL and LDL cholesterol levels increased significantly in each group. No significant differences were observed with respect to extent of these changes between the groups. Thus, although lipid levels at the time of angioplasty and at 6 months follow-up were not found to predict the occurrence of restenosis, the association of low high-density lipoprotein levels and the tendency for restenosis should not be overlooked.

Priming of Peyer's patch lymphoid cells by hemorrhagic shock and resuscitation to produce superoxide radical.

Hemorrhagic shock (HS) can cause whole body ischemia including the gastrointestinal tract. We investigated whether cells from small intestine Peyer's patches (PP) were capable of producing superoxide radical when animals underwent HS or HS followed by resuscitation (HS/RS). HS was initiated by removing 60% of the blood volume of surgically prepared guinea pigs. PP lymphoid cells were purified and stimulated with phorbol 12-myristate 13-acetate in the presence of spin trap 5-diethoxyphosphoryl-5-methyl-1-pyrroline-N-oxide (DEPMPO). Electron paramagnetic resonance spectra of PP lymphoid cells from sham-treated control, HS, and HS/RS animals produced DEPMPO radical adducts characterized as the adducts of superoxide (DEPMPO/*OOH) and hydroxyl (DEPMPO/*OH) radicals. The formation of both radical adducts was totally inhibited by superoxide dismutase or a nicotinamide adenine dinucleotide phosphate (reduced form) oxidase inhibitor, diphenyleneiodonium chloride. HS/RS increased radical adduct formation, expressed as a percentage control, by 160% and 225% for DEPMPO/*OOH, and DEPMPO/*OH, respectively. When animals were allowed to recover for 24 h post-HS/RS treatment, PP cells decreased the superoxide generation to the same level as controls. Thus, RS following HS may prime PP lymphoid cells for increased nicotinamide adenine dinucleotide phosphate (reduced form) oxidase-dependent superoxide generation, and this process may have cytotoxic and/or immunomodulatory effects on the host.

Effects of endotoxin on the guinea pig heart response to ischemia reperfusion injury.

Ischemia causes significant damage to the heart as manifested by decreases in ventricular performance. Several different methods have been shown to protect the heart from ischemic injury--one is operative over a short period (an hour) and the other over longer periods (a day). The latter form of protection has been demonstrated in rats after induction of Gram-negative sepsis or administration of endotoxin or cytokines. In the present study we determined whether guinea pigs would also show induction of cardiac protection subsequent to a dose of endotoxin. Male guinea pigs were injected with 1 mg of endotoxin and studied the following day. Hearts were perfused at a constant perfusion pressure and studied in an isovolumic mode. Left ventricular developed pressure was significantly lower in the endotoxin-treated group than in the control group. After 35 min of total ischemia and 25 min of reperfusion, recovery of left ventricular developed pressure was complete in the endotoxin group but significantly decreased in the control group such that after ischemia and reperfusion, there was no significant difference in left ventricular performance between the two groups. Coronary flow was significantly greater in the endotoxin group than in the control group both prior to and after ischemia. Hearts from endotoxin-treated guinea pigs resumed spontaneous contractile activity sooner and released less lactate upon reperfusion than did the control group. Thus prior treatment of guinea pigs with endotoxin resulted in depression of the isolated heart but also resulted in protection of the isolated heart from further damage due to ischemia/reperfusion injury.